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Non-Coding RNAs in Breast Cancer: Intracellular and Intercellular Communication

Carolyn M. Klinge

Non-Coding RNA · 2018 · Review · CC BY

doi:10.3390/ncrna4040040

Abstract

Non-coding RNAs (ncRNAs) are regulators of intracellular and intercellular signaling in breast cancer. ncRNAs modulate intracellular signaling to control diverse cellular processes, including levels and activity of estrogen receptor α (ERα), proliferation, invasion, migration, apoptosis, and stemness. In addition, ncRNAs can be packaged into exosomes to provide intercellular communication by the transmission of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) to cells locally or systemically. This review provides an overview of the biogenesis and roles of ncRNAs: small nucleolar RNA (snRNA), circular RNAs (circRNAs), PIWI-interacting RNAs (piRNAs), miRNAs, and lncRNAs in breast cancer. Since more is known about the miRNAs and lncRNAs that are expressed in breast tumors, their established targets as oncogenic drivers and tumor suppressors will be reviewed. The focus is on miRNAs and lncRNAs identified in breast tumors, since a number of ncRNAs identified in breast cancer cells are not dysregulated in breast tumors. The identity and putative function of selected lncRNAs increased: nuclear paraspeckle assembly transcript 1 (NEAT1), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), steroid receptor RNA activator 1 (SRA1), colon cancer associated transcript 2 (CCAT2), colorectal neoplasia differentially expressed (CRNDE), myocardial infarction associated transcript (MIAT), and long intergenic non-protein coding RNA, Regulator of Reprogramming (LINC-ROR); and decreased levels of maternally-expressed 3 (MEG3) in breast tumors have been observed as well. miRNAs and lncRNAs are considered targets of therapeutic intervention in breast cancer, but further work is needed to bring the promise of regulating their activities to clinical use.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 26, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

Breast cancer is the most commonly diagnosed cancer and second leading cause of cancer death among women in the United States (U.S.). Breast tumors are heterogeneous, and are pathologically classified according to their expression of key proteins by immunohistochemical (IHC) staining (at a minimum 1%): estrogen receptor α (ERα), gene ESR1, tumors are termed ER positive (ER+), progesterone receptor (PR, gene PGR), and human epidermal growth factor receptor 2 (HER2, gene ERBB2). Tumors that lack these three protein markers are “basal-like” and referred to as triple negative breast cancer (TNBC). Most primary breast tumors are ER+/PR+/HER2-, and patients are treated with surgery, radiation, and endocrine therapies (also referred to as antiestrogen therapies) Endocrine therapies employ aromatase inhibitors (AI), e.g., letrozole, to block the conversion of androgens to estrogens, or tamoxifen (TAM), which is a selective ER modulator (SERM) that competes with estrogens, including estradiol (E2) for binding ER. Most postmenopausal women with ER+ breast tumors receive AI therapy, while American Society of Clinical Oncology (ASCO) guidelines recommend 10 years of TAM for premenopausal women. Unfortunately, 30–40% of patients develop resistance to endocrine therapies and develop metastatic disease. Multiple mechanisms are involved in acquired endocrine resistant breast cancer. Approximately 25–40% of metastatic tumors in breast cancer patients treated with AIs show ESR1 mutations within the ligand binding domain (LBD). These mutations result in the ligand-independent transcriptional activity of the mutant ERα and reduce the efficacy of ER antagonists, including the selective ER downregulators (SERDs) fulvestrant, AZD9496, RU-58688, and GDC-0810. Both ESR1 Y537S and D538G mutations are associated with more aggressive disease biology and shorter survival. Recent clinical data suggest that the addition of the CDK4/6 inhibitor palbociclib in combination with letrozole provides a benefit in advanced disease. Gene expression analysis in primary breast tumors for 50 genes in the PAM50 test has allowed the further dissection of molecular phenotypes that have clinical implications for individualizing patient treatment. As of yet, no non-coding RNAs (ncRNAs) are used in commercial diagnostic tests; however, there is great interest in identifying circulating microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in breast cancer diagnosis and for monitoring therapeutic response.

Over the past two decades, we have learned that 99% of the total cellular RNA content of human cells consists of ncRNAs that are classified by size and function. Transfer RNA (tRNA) (89%) and ribosomal RNA (rRNA) (8.9%) constitute the majority of ncRNAs, followed in abundance by messenger RNAs (mRNAs) (0.9%). Thus, the remaining ncRNAs, including circular RNA (circRNA), small nuclear RNA (snRNA), small nucleolar RNA (snoRNA), miRNA, and lncRNA together account for ~1% of total ncRNA. Despite their low abundance, these ncRNAs play critical roles in transcription, post-transcriptional processing, and translation. In addition, because ncRNA can be packaged into extracellular vesicles (EV), including exosomes, they provide a mechanism for intercellular communication by the transfer of miRNA and lncRNA to recipient cells both locally and systemically. It is important to note that the levels of ncRNA expression, their post-transcriptional modification (particularly lncRNAs), and their subcellular distribution are important to consider in assigning their potential function. As concluded by Palazzo and Lee, it is ultimately critical to examine the biological function of each identified ncRNA on a case-by-case basis. Table 1 lists the best-characterized regulatory ncRNAs with roles in breast cancer, as well as their sizes and function.

LncRNAs and miRNAs are considered to be epigenetic regulators of human cancers. Both pri-miRNAs and lncRNAs are post-transcriptionally modified, e.g., by the methylation on N6 of adenosine (m6A), which alters their activities, providing an additional layer of regulation termed “epitranscriptomics”. In addition, there is one report that a pool of inactive miR-34 lacking the 5′-phosphate in cancer cells, including MCF-7 cells, is activated by 5′-end phosphorylation by ATM serine/threonine kinase (ATM) and cleavage and polyadenylation factor I subunit 1 (CLP1) in response to DNA damage, in turn allowing AGO2 loading. At least three times more reports are listed in PubMed on miRNAs than lncRNAs in endocrine cancers.

2. Small Nuclear RNAs and Small Nucleolar RNAs in Breast Cancer

snRNAs and snoRNAs play roles in mRNA splicing and rRNA maturation, respectively (reviewed in). Elevated snoRNA biogenesis is required for the high rRNA expression that is needed for ribosomal biogenesis and enhanced protein synthesis in breast cancer (reviewed in). Some snoRNAs are expressed in a cell-specific manner, including SNORD46 and SNORD42A in mammary glands and lymphoblastoid cells in the ENCODE (Encyclopedia of DNA elements) dataset (reviewed in). Thirteen snoRNAs were identified as having prognostic relevance in breast cancer, including the downregulation of SNORD46 and SNORD89. The clonal evolution of successful cancer cells is guided by intracellular and intercellular mutations that provide advantages or disadvantages to cell lineages. This evolution is mediated in part by ribosomal alterations that are driven by mutations in uL18/RPL5 ribosomal protein genes in ~34% of breast tumors. Many snoRNAs are processed into stable miRNA-like oligomers that are called ‘small nucleolar RNA-derived RNAs’ (sdRNAs). sdRNA-93 was reported to play a role in MDA-MB-231 cell invasiveness, and is overexpressed in Luminal B/HER2+ breast tumors relative to other types of breast tumors or normal breast tissue. Other studies show that alterations in snoRNAs may promote carcinogenesis and favor caner stem cell phenotypes.

3. Circular RNAs

During the splicing of exons and removal of introns from heterogeneous nuclear RNA (hnRNA) to generate mRNA, “backsplicing” can generate circular RNAs (circRNAs) that are usually exported to the cytoplasm. CircRNAs are considered stable, although they are expressed at <10% of their associated linear mRNA transcripts (reviewed in). circRNAs are evolutionarily conserved, suggesting that they are critical for cellular activities. Several factors regulate circRNA levels, including exon-skipping events, complementary sequences of flanking introns, RNA-binding proteins, and the amount of more than 25 of the ~170 proteins that constitute the spliceosome. circRNAs can act as competing endogenous RNA (ceRNA, also called ‘sponge’) for microRNAs, thus reducing miRNA repression of their target mRNAs. circRNAs modulate the stability of mRNAs, interact with RNA binding proteins, and regulate gene transcription by interaction with RNA pol II. In addition, recent studies show that some circRNAs are translated, including circ-SHPRH, which generates a 17 kDa SHPRH-146aa protein that acts as a novel tumor suppressor protein and a protective decoy for its full-length SHPRH protein in glioblastoma.

At least six circRNAs have been reported as having roles in breast cancer (Table 1). Examples of circRNAs that are increased in breast tumors and classified as having oncogenic activity in breast cancer cell lines by acting as ceRNA for miRNAs include: hsa_circ_ABCB10 (ceRNA for miR-1271); hsa_circ_0011946 (ceRNA for miR-26a/b and thus upregulating RFC3 in MCF-7 cells), hsa_circ_0052112 (ceRNA for miR-125a-5p in MDA-MB-231 cells), and hsa_circ_0008039 (ceRNA for miR-432-5p and thus increasing E2F3 expression in MCF-7 and BT-20 cells). Recently, hsa_circ_0007294 (circANKS1B) was shown to be upregulated in TNBC tumors compared with all other breast tumor types, and circANKS1B acts as a ceRNA for miR-148a-3p and miR-152-3p, resulting in the increased expression of USF1, which increases transforming growth factor β1 (TGF-β1) expression to stimulate epithelial-to-mesenchymal transformation (EMT). It is likely that the further examination of RNA profiling data will identify more circRNAs in breast tumors, which will necessitate further molecular and functional studies about their roles in tumor formation, progression, and metastasis.

4. PIWI-Interacting RNAs

piRNAs work in PIWI–piRNA complexes to regulate gene expression at the epigenetic and post-transcriptional levels. piRNAs are the guardians of genome integrity by epigenetically silencing transposable elements by DNA methylation. PIWI proteins are aberrantly expressed in breast cancer, including a high expression of PIWIL2, which is a member of the PIWI/AGO gene family, and PIWIL4 is highly expressed in TNBC tumors and cell lines, and correlates with distant metastasis fatality. Experiments in MDA-MB-231 TNBC cells demonstrated that PIWIL4 activates TGF-β, MAPK/ERK, and fibroblast growth factor (FGF) signaling, and suppresses the expression of MHC class II genes. The analysis of existing small RNAs in–RNA seq data identified >100 piRNAs in breast cancer cells, some of which were differentially expressed in MCF-7, ZR-75.1, and SKBR3 breast cancer cells relative to MCF-10A immortalized ‘normal’ breast epithelial cells. The role of piRNAs in breast tumors remains to be thoroughly examined.

5. MicroRNAs in Breast Cancer

Reflecting the intense interest in the role of miRNAs in breast cancer initiation, progression, and metastasis, there are currently ~3662 publications on miRNAs in breast cancer in PubMed. The reason behind this interest is that miRNAs are dysregulated in breast cancer (reviewed in). Since each miRNA has the theoretical capacity to regulate multiple gene targets post-transcriptionally, alteration in the expression levels of just one miRNA has the potential to affect hundreds of target mRNAs. There are a number of programs to identify targets of a selected miRNA, and conversely, the miRNAs that may regulate a specific target gene (mRNA). Examples include miRTarBase, PicTar, miRanda, and MirAncesTar, although these programs predict false positives and false negatives (reviewed in). Thus, experimental verification of the ability of a miRNA to downregulate a target requires cloning the 3′UTR of the target mRNA downstream of a luciferase reporter driven by an active promoter, e.g., CMV, mutating the miRNA recognition element in the reporter, and performing transient transfection assays in cells using the overexpression of wild-type miRNA and knockdown the miRNA expression. In addition, westerns and/or immunohistochemical staining (IHC) are needed to validate the decrease in authenticated target protein expression.

miRNAs are short (~22 nt) single-stranded RNAs that regulate mRNA stability and/or translation by base-pairing between the seed sequences at 5′ positions 2–7 or 2–8 of the miRNA with ~7 bp miRNA recognition elements (MREs) in the 3’UTR of their target mRNAs within the RNA-induced silencing complex (RISC). The current miRBase (release 22) reports 2654 mature miRNAs (http://www.mirbase.org/). Additional complexity is offered by the production of isomiRs that are generated from a single miRNA locus by template and non-template variants, and are differentially expressed in different types of human breast tumors. The biogenesis of miRNAs has been extensively reviewed. In summary, most miRNAs are transcribed as primary (pri)-miRNAs by RNA polymerase II, either cotranscribed within introns of host genes or as independent genes, and processed within the nucleus by the DROSHA-DGCR8 microprocessor complex. DROSHA cleaves the hairpin-loop pri-miRNA yielding a 60–70 nt precursor (pre)-miRNA that is exported from the nucleus by the Exportin (XPO5) and Ran-GTP (RAN) or Exportin1 (XPO1, also called CRM1). The high/middle methylation of XPO5 was associated with reduced breast cancer risk, and XPO5 expression is increased in breast tumors. An epidemiological study of key miRNA processing genes in the blood of male U.S. veterans reported that the DNA methylation of DROSHA and TNRC6B may play a role in early carcinogenesis. DROSHA has tumor suppressor or oncogenic activity, depending on the type of tumor (reviewed in). Single nucleotide polymorphisms (SNPs) in DROSHA are associated with increased breast cancer risk. In the cytoplasm, the DICER-TRBP complex unwinds the double-stranded precursor miRNA (pre-miRNA) to allow the incorporation of one strand of the miRNA (called the guide strand) into the RISC complex that includes the catalytic Argonaut proteins, e.g., AGO2. The non-incorporated passenger strand of miRNA is degraded. DICER is considered a tumor suppressor in breast cancer. Increased DICER was associated with TAM resistance in metastatic breast tumors and tumor xenografts. The high expression of AGO2 was reported to correlate with the luminal B subtype of breast cancer. Interestingly, the overexpression of AGO2 in MCF-7 human breast cancer cells increased the expression of an ERα variant called ERα36, and stimulated E2-induced xenograft tumor growth in vivo in severe combined immunodeficiency (SCID)/Beige female mice. This observation is of interest, since ERα36 plays a role in endocrine resistance and cancer stem cells (CSC) in breast cancer.

Next-generation sequencing approaches have identified ‘mitomiRs’ that function in mitochondria, whether by being imported from the repertoire of nuclear-encoded miRNAs or transcribed from the mitochondrial DNA (mtDNA). miRNAs may act as retrograde and anterograde signaling molecules between mitochondria and the nucleus to regulate energy homeostasis and apoptosis. However, caution is needed, since the cytosolic contamination of mitochondrial extracts can lead to artifacts. The role of mitomiRs in breast cancer is unknown. It is intriguing to note that PyMT mammary tumor metastasis was regulated by mtDNA in transgenic “mitochondrial-nuclear exchange (MNX) mice”, i.e., mice that had BL/6 mitochondria had longer tumor latency compared to those with FVB or BALB/c mitochondria, and mice with BALB/c mitochondria showed higher metastatic areas in lung. At present, the precise mechanism(s) for this observation remain to be determined.

miRNAs that are overexpressed in breast tumor are called ‘oncomiRs’, since they promote carcinogenesis and progression by downregulating tumor suppressor genes. One example of an oncomiR in breast, as well as many cancers, is miR-21. Some examples of validated targets of miR-21 are indicated in Table 2. On the other hand, miRNAs that are downregulated in breast tumors are called tumor suppressor miRNAs. Notably, it is incorrect to assume that a miRNA is always an oncomiR or a tumor suppressor miRNA, since the activity of each miRNA depends on the cellular context, which includes mitigating factors such as lncRNAs and circRNAs (reviewed in). It is important to note that many of the miRNAs that have been studied in breast cancer cell lines (reviewed in) are not dysregulated in human breast tumors; thus, the focus here is on those identified in human breast tumors.

In breast cancer, miRNAs regulate genes involved in apoptosis, cell-signaling pathways (e.g., TGFβ, epithelial-to-mesenchymal transformation (EMT), metastasis, the expression of ERα and other nuclear receptors (NRs)), regulation of the tumor microenvironment, and stemness, which includes transfer or exosomal miRNAs to adjacent normal fibroblasts forming cancer-associated fibroblasts (CAFs) (reviewed in). Figure 1, Figure 2 and Figure 3 highlight the pathways of some of the miRNAs dysregulated in breast cancer, as summarized in Table 2 and Table 3. In addition, the lncRNAs that have been reported to ‘sponge’ some of the dysregulated miRNAs are shown as competing endogenous RNA (ceRNA).

Croce’s group first identified miRNAs dysregulated in breast cancer in 2005. There are numerous reviews covering 13 years of publications on the identity, targets, and regulation of miRNAs in breast cancer, and these references are not fully inclusive of all the published work. The identity and possible roles of miRNA dysregulated in specific subtypes of breast cancer, including HER2+, TNBC, and endocrine-resistant breast cancer have been reviewed.

6. Long Non-Coding RNAs in Breast Cancer

The current GENECODE (version 28, GRCh38.p12) of the human genome includes 58,381 genes, 15,779 long non-coding RNAs (lncRNAs), and 1881 miRNAs (https://www.gencodegenes.org/stats/archive.html#a28). LncRNAs are defined as ncRNAs of >200 nucleotides. They are transcribed from genomic DNA by RNA pol II, and are classified according to the genomic organization: (1) intergenic lncRNAs (lincRNAs) are transcribed between two protein-coding genes; (2) intronic lncRNAs are transcribed from the introns of protein-coding genes; (3) overlapping lncRNAs, which overlap protein-coding genes; and 4) antisense (as) lncRNAs, which are transcribed in a direction opposite to that of the protein-coding gene. lncRNA expression is a low percent of total cellular RNA, i.e., ~0.03–0.20%. Thus, while 15,779 lncRNAs have been identified, very few have been characterized with respect to cell type specificity and function. There is a need to develop tools for an improved analysis of differentially expressed lncRNAs. Since lncRNAs are low in expression, their expression levels are “very noisy”, which reflects their low counts in RNA-seq data. Overall, quantitative examination of the identity of lncRNAs and their roles is needed, including in breast cancer.

In addition to nuclear-encoded lncRNAs, seven lncRNAs were identified as mitochondrial DNA transcripts mtDNA. Two lncRNAs are encoded by mitochondrial D-loop regions: MDL1 and MDL1AS. There is evidence of mt-encoded lncRNAs in the nucleus, suggesting a potential role in retrograde signaling; however, there are no reports on mtDNA-encoded lncRNAs in breast cancer.

Functionally, lncRNAs regulate transcription by associating with enhancer regions, in cis, i.e., at adjacent sites relative to their own transcription, or in trans, i.e., at more distal sites. lncRNAs have heterogeneous complex 3D structures, which allows them to assume different shapes and interact with a wide variety of intracellular components. lncRNAs interact with the Mediator complex, forming loops between enhancer and promoter regions. lncRNAs interact with proteins and other RNAs to influence their activities and cellular location. lncRNAs regulate development and differentiation, gene imprinting, and antiviral responses; and assist in chromatin modification, mRNA splicing, and protein stability. Another function of lncRNAs is to act as ‘sponges’ (ceRNAs) for miRNAs, thus blocking the repressive activity of miRNAs for binding to the 3’UTR of their target transcripts. A network analysis of ncRNAs in cancer drug resistance-associated lncRNAs–miRNAs, TAM resistance (including lncRNAs MALAT1 and CCAT2; miR-221, miR-222, miR-26a, miR29a, miR-29b), and Trastuzumab resistance (lncRNA GAS5, miR-16, and miR-155) has been described. lncRNAs act as scaffolds, e.g., HOTAIR links the PRC2 and LSD1 histone-modifying complexes to promote histone H3K27 methylation and H3K4 demethylation to silence target genes and promote breast cancer metastasis.

The identity and roles of lncRNAs in breast cancer have been reviewed. lncRNA expression profiles have been correlated with hormone status and intrinsic tumor type. At present, there is no consistent identification of which lncRNAs in primary tumors are the best signature for predicting patient outcomes. For example, using four Gene Expression Omnibus (GEO) datasets (n = 473 breast cancer patients), one group identified a 12-lncRNA predictive signature for recurrence (RP1-34M23.5, RP11-202K23.1, RP11-560G2.1, RP4-591L5.2, RP13-104F24.2, RP11-506D12.5, ERVH48-1, RP4-613B23.1, RP11-360F5.1, CTD-2031P19.5, RP11-247A12.8, and SNHG7), and another group using TCGA (n = 1064) identified a different set of three lncRNAs as prognostic markers (CAT104, LINC01234, and STXBP5-AS1). The differences may be the result of different platforms—the Affymetrix HG-U133 Plus 2.0 platform versus RNA-seq—in addition to the different tumors analyzed, the heterogeneity of breast tumors, the method of lncRNA identification and data interrogation, and, as stated earlier, the low level of lncRNA expression that confounds statistically relevant data interpretation. For this review, a selection of nuclear encoded lncRNAs that have been identified as dysregulated in breast tumors will be briefly summarized.

The lncRNA RMRP (RNA component of mitochondrial RNA processing endoribonuclease) binds RNA-binding proteins GRSF1, HUR, and PNPASE for transport into mitochondria, where RMRP plays a role in RNA processing and mtDNA replication. Mutations were identified in the promoters of lncRNAs RMRP and nuclear paraspeckle assembly transcript 1 (NEAT1) that increased their expression in human breast tumors. However, the expression of NEAT1 showed no correlation with clinical gene signatures associated with higher grade, stage, metastasis, tumor aggression, or TAM resistance. Thus, the role of NEAT1 in breast cancer is unclear. Patients whose primary breast tumors showed a high expression of NEAT1, colon cancer associated transcript 2 (CCAT2), or metastasis associated lung adenocarcinoma transcript 1 (MALAT1) had shorter overall survival (OS).

NEAT1 is involved in the organization of nuclear architecture called paraspeckles for gene transcription and splicing. Nuclear speckles are dynamic punctate compartments in the nucleus that contain components of the pre-mRNA spliceosome, including SRSFs, small nuclear ribonucleoproteins (snRNPs), RNA Pol II subunits, 3’ end processing proteins, m6A writers METTL3/14 and reader YTHDC1, and various protein kinases that regulate the pool of proteins in the speckles. NEAT1 was identified as an essential component of the FOXN3–SIN3A repressor complex, and the overexpression of NEAT1 promoted EMT in ERα+ MCF-7 breast cancer cells and promoted the lung metastasis of MCF-7 when orthotopically implanted in the mammary fat pad, suggesting that NEAT1 has oncogenic activity. Bioinformatic analysis of sample-matched miRNA-seq and RNA-SeqV2 data of breast cancer from The Cancer Genome Atlas (TCGA) revealed that NEAT1 was overexpressed in luminal A, luminal B, HER2+, and basal-like (TNBC) tumors. Further, the authors identified a putative ceRNA network for NEAT1, as well as lncRNAs OPI5-AS1 and AC008124.1 in all breast tumors and each subtype. NEAT1 was also identified in a gene (ESR1, DKC1)–lncRNA (TERC and TUG1) interaction network in breast tumors from TCGA.

Another integrative analysis of RNA-seq data of ~1000 breast tumors in TCGA identified GATA3-AS1 (ENSG00000197308), RP11-279F6 (ENSG00000245750), and AC017048 as highly expressed in ERα-positive versus ERα-negative breast tumors and normal breast tissue samples. However, there are no confirming reports on these three lncRNAs or their function in breast cancer. Another analysis of TGCA RNA-seq data of human breast tumors identified a decreased expression of LINC00092 and C2orf71 as associated with poor prognosis, and identified a putative network of coexpression of LINC00092 with mRNAs RGMA and SFRP1 that were regulated by miR-449a and miR-452-5p. However, neither of these miRNAs were dysregulated in breast tumors. Further, C2orf71 has been identified as a protein-coding gene PCARE in GeneCards.

The lncRNA SRA1, which is a steroid receptor RNA activator, was first identified in a complex with the coactivator SRC-1 (NCOA1) as an RNA coactivator that increased the transcriptional activity of NR, including ERα. SRA1 expression was higher in breast tumors compared with adjacent normal breast tissue. SRA1 is unique in that not only does it encode lncSRA1s of different length, but SRA1 also encodes a protein: steroid receptor co-activator protein (SRAP) (reviewed in). SRAP does not interact with the lncRNA SRA1, but it interacts with NRs: ERα, androgen receptor (AR), and glucocorticoid receptor (GR), and is involved in splicing and cell cycle regulation. The lncRNA SRA1 functions as a scaffold, and interacts with miRNA processing (DICER and TRBP) and RISC components, i.e., AGO2 and PACT; with other transcription factors, e.g., OCT4, NANOG, and FOXO1; and with chromatin modifiers and binding proteins, e.g., KMT2A (MLL1), KMT2D (MLL2), EZH2, and CTCF.

MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) is one of the best characterized lncRNAs with roles in neural development and function, retina, myogenesis, and vascular cell proliferation; it is dysregulated in cancers, including upregulation in breast tumors (reviewed in). Serum levels of MALAT1, as examined by quantitative real-time PCR (qPCR), were higher in breast cancer patients (n = 157) than normal women (n = 107). MALAT1 expression is associated with ERα+/PR+ breast tumors and with lower relapse-free survival (RFS). MALAT1 staining was also higher in formalin-fixed paraffin embedded (FFPE) breast tumors than normal tissue. MALAT1 is oncogenic in breast cancer, and it upregulates the WNT/β-catenin (CTNNB1) pathway. MALAT1 mutations are frequent in breast tumors. MALAT1 acts as a ceRNA for miR-9, miR-133, miR-145, miR-195, miR-200s, miR-205, miR-206, and miR-503 (reviewed in). MALAT1 is targeted by interaction with miR-101, miR-125b, and miR-217. MALAT1 acts as scaffold to position nuclear speckles at active gene loci. Capture hybridization analysis of RNA targets (CHART) revealed binding of MALAT1 at actively transcribed loci (reviewed in. Proteins interacting with MALAT1 were identified by SILAC (stable isotope labeling with amino acids) labeling and LC-MS/MS proteomics in HEPG2 human hepatoma cells, and included proteins involved in RNA processing, splicing and gene transcription, and HNRNPAB. Despite its lower expression in HER2+ and TNBC tumors, MALAT1 expression was associated with decreased disease-specific survival in these patients. Despite these studies implicating MALAT1 as oncogenic, a recent study in MMTV-PyMT;Malat1−/− mice demonstrated that MALAT1 is a suppressor of lung metastasis in this model. Notably, there was no difference in overall survival or tumor weight in the MMTV-PyMT;Malat1+/+ versus MMTV-PyMT;Malat1−/− mice and no difference in histological metrics of the tumors. The authors also reported that in TCGA RNA seq data, MALAT1 was “underexpressed in human breast tumors compared with normal breast tissue”, and that lower MALAT1 levels correlated with shorter distant metastasis-free survival in all breast cancer, as well as in luminal A and basal breast cancer. Using chromatin isolation by RNA purification coupled to mass spectrometry (ChIRP-MS) studies, they demonstrated that Malat1 sequestered the transcription factor TEAD, thus inhibiting its activity in mouse mammary tumors.

The expression of the lncRNA CCAT2 (Colon Cancer Associated Transcript 2) is increased in breast tumors and breast cancer cells relative to normal breast tissue/cells. Knockdown of CCAT2 inhibited MCF-7 and MDA-MB-231 breast cancer cell proliferation and invasion in transwell migration assays by inhibiting WNT/β-catenin signaling. CCAT2 expression was higher in MDA-MB-231 and LCC9 TAM-resistant breast cancer cells derived from MCF-7 cells than in parental MCF-7 cells, and knockdown of CCAT2 inhibited the activation of TGFβ signaling in LCC9 and MCF-7 cells. CCAT2 was reported to bind EZH2 and increased H3K27me3 in chromatin, thus repressing CDKN2B transcript and protein expression in MDA-MB-231 cells. CDKN2B encodes a cyclin-dependent kinase inhibitor that interacts with CDK4 or CDK6, thus preventing interaction with cyclin D and inhibiting G1-S cell cycle progression. Thus, the repression of CDKN2B would allow cell cycle progression. These results are as of yet unconfirmed in human breast tumors. The authors suggest the potential for therapeutic agents targeting cellular pathways linked to MALAT1.

Levels of the lncRNA CRNDE (colorectal neoplasia differentially expressed) were higher in breast tumors than normal breast and correlated with reduced OS. CRNDE is a ceRNA for miR-136, resulting in the activation of WNT/β-catenin signaling in MDA-MB-231 cells. Wnt signaling is a key driver of stem cells in embryonic and adult tissues and CSCs.

Analysis of TCGA breast tumor data identified higher expression of the lncRNA MIAT (myocardial infarction associated transcript) in breast tumors than normal breast tissue. MIAT is a ceRNA for miR-155-5p, and knockdown of MIAT increased expression of the miR-155-5p target DUSP7 and inhibited MDA-MB-231 cell proliferation and xenograft tumor growth.

The lncRNA LINC-ROR was discovered in pluripotent stem cells, where it functions as a ceRNA for miR-145 to increase key pluripotency transcription factors OCT4, NANOG, and SOX2. LINC-ROR expression was higher in breast tumors and cell lines relative to normal breast tissue, and MCF-10A cells and the overexpression of LINC-ROR induced markers of EMT in MCF-10A cells. High LINC-ROR expression in breast tumors was associated with reduced OS, and knockdown of LINC-ROR inhibited TGFβ signaling in MCF-7 and MDA-MB-231 cells. Whether LINC-ROR is involved in the stimulation of CSC or metastasis remains to be examined.

Conversely, the expression of MEG3 (Maternally Expressed 3) is lower in breast tumors than in normal breast tissues, and the expression level of MEG3 was negatively correlated with histological tumor grade, and MEG3 downregulation correlated with poor OS. MEG3 is a ceRNA for miR-421 in MDA-MB-231 TNBC and increased E-cadherin, while decreasing cell invasion in vitro. The overexpression of MEG3 in MDA-MB-231 cells suppressed xenograft tumor growth and angiogenesis, and reduced P-AKT, PCNA, and MMP-9 protein expression in the tumors formed in the mice. Whether MEG3 could be a potential therapy in breast cancer is not yet known, but is of interest in nervous system cancers.

lncRNAs continue to be discovered through the bioinformatic analysis of breast tumor data. For example, a recently published analysis of TCGA breast tumor identified putative driver lncRNAs: the amplification of AC084809.2, RP11-108P20.3, ACOO5076.5, RP11-385J1.2, RP11-567G11.1, LINC00909, ATP1B3-AS1, MCCC1-AS1, YEATS2-AS1, TP53TG1, and SOX2-OT. As suggested previously, much more research is needed to understand the roles of lncRNAs in breast cancer initiation, progression, and metastasis.

7. Micro RNAs and Long Non-Coding RNAs in Extracellular Vesicles and Exosomes

Exosomes are a type of extracellular vesicle (EV) that are ~50–140 nm in size, endosome-derived, and secreted by most cells under normal and disease states. Surface markers on exosomes include CD9, CD63, CD81, LAMP1, and TSG101. Microvesicles (MVs, also called ‘ectosomes’) are EVs that bud from the plasma membrane surface, but many people refer to MVs and exosomes interchangeably. Exosomes contain ncRNA (circRNA, miRNA, lncRNA) in addition to dsDNA, mRNA, proteins, lipids, DICER, and TRBP, as well as AGO2, and process pre-miRNAs to mature miRNAs. A web-based database exoRBase is a repository of 15,501 lncRNA, 58,330 circRNA, and 18,333 mRNA. Exosome levels are higher in the serum of breast cancer patients compared to normal subjects. EVs deliver cargo, including ncRNA, lipids, mtDNA, and proteins, between cells and play roles in the context of tumor growth and the stimulation of metastasis while suppressing immune detection. EVs, and exosomes in particular, are considered of great promise as ‘liquid biopsy’ and biomarkers in cancer detection and monitoring therapeutic response. Examples of exosomal miRNAs that are released by breast cancer cells and found in higher amount in the serum of breast cancer patients than controls include miR-21, miR-195, miR-484, and miR 1246. However, there is concern about the manner of sample collection and variability in content of EVs, and exosomes due to different methods of isolation that are yet to be standardized for clinical lab testing.

The role of exosomal miRNAs in breast cancer has been reviewed. Exosomes are secreted by cancer cells and by cancer-associated fibroblasts, and can be taken up by neighboring cells in the tumor environment, including NK cells and T lymphocytes, as well as distant cells after traveling in blood. Examples of exosomal miRNAs and their targets in breast cancer are shown in Figure 4. Exosomes secreted from TAM-resistant MCF-7 cells in vitro were shown to confer TAM resistance to parental MCF-7 cells, in part by delivering miR-222 and miR-221 that repress ESR1 (ERα) translation. Exosomes from TAM-resistant LCC2 cells, derived from MCF-7 cells, had higher levels of the lncRNA UCA1 than parental MCF-7 cells, and the incubation of MCF-7 cells with exosomes from LCC2 cells conferred TAM-resistance. We reported that miR-29b-1/a directly targets ATP synthase subunit genes ATP5G1 and ATPIF1 and inhibit OCR and decrease ATP in MCF-7 and LCC9 breast cancer cells. UCA1 activates AKT-mTOR signaling and is a ceRNA for miR-18a, thus derepressing HIF-1α. The lncRNA MALAT1 is found in exosomes from breast cancer patients. MALAT1 is known to activate WNT–β-catenin signaling, and is oncogenic in breast cancer (reviewed in). Most studies have characterized the activities of miRNAs and lncRNAs in cancer cell exosomes in vitro; thus, research is needed to validate the role of these miRNAs and lncRNAs in breast cancer metastasis in vivo.

8. Concluding Considerations

ncRNAs are dysregulated in breast cancer and miRNAs, noted for their stability, and lncRNAs are being investigated as biomarkers of disease pathology, prognostic indicators, and potential therapeutic targets, as well as modalities to block cancer progression and metastasis. We know much more about miRNAs than lncRNAs in human breast tumors. Our understanding of the networks between miRNAs, lncRNAs, their interacting partners, and targets is expanding. However, individual and combinations of miRNAs and lncRNAs have cell-specific activities that are not fully understood, nor is their interaction with the immune system, microbiome, microenvironment, hormonal milieu, or metabolome elucidated. Further investigation is needed to bring studies on miRNAs and lncRNAs into clinical practice for diagnosis, prognosis, and therapeutics in breast cancer patients.

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    Not in our library10.1158/1055-9965.epi-17-0849

  95. 95.

    Hata A., Kashima R. Dysregulation of microRNA biogenesis machinery in cancer. Crit. Rev. Biochem. Mol. Biol. 2016;51:121-134.

    Not in our library10.3109/10409238.2015.1117054

  96. 96.

    Khan S., Greco D., Michailidou K., Milne R.L., Muranen T.A., Heikkinen T., Aaltonen K., Dennis J., Bolla M.K., Liu J., et al. MicroRNA Related Polymorphisms and Breast Cancer Risk. PLoS ONE. 2014;9:e109973.

    Not in our library10.1371/journal.pone.0109973

  97. 97.

    Hock J., Meister G. The Argonaute protein family. Genome Biol. 2008;9:210.

    Not in our library10.1186/gb-2008-9-2-210

  98. 98.

    Pitchiaya S., Heinicke L.A., Park J.I., Cameron E.L., Walter N.G. Resolving Subcellular miRNA Trafficking and Turnover at Single-Molecule Resolution. Cell Rep. 2017;19:630-642.

    Not in our library10.1016/j.celrep.2017.03.075

  99. 99.

    Selever J., Gu G., Lewis M.T., Beyer A., Herynk M.H., Covington K.R., Tsimelzon A., Dontu G., Provost P., Di Pietro A., et al. Dicer-Mediated Upregulation of BCRP Confers Tamoxifen Resistance in Human Breast Cancer Cells. Clin. Cancer Res. 2011;17:6510-6521.

    Not in our library10.1158/1078-0432.ccr-11-1403

  100. 100.

    Conger A.K., Martin E.C., Yan T.J., Rhodes L.V., Hoang V.T., La J., Anbalagan M., Burks H.E., Rowan B.G., Nephew K.P., et al. Argonaute 2 Expression Correlates with a Luminal B Breast Cancer Subtype and Induces Estrogen Receptor Alpha Isoform Variation. Non-Codin. RNA. 2016;2:8.

    Not in our library10.3390/ncrna2030008

  101. 101.

    Wang Z.-Y., Yin L. Estrogen receptor alpha-36 (ER-α36): A new player in human breast cancer. Mol. Cell Endocrinol. 2015;418:193-206.

    Not in our library10.1016/j.mce.2015.04.017

  102. 102.

    Vendramin R., Marine J.C., Leucci E. Non-coding RNAs: The dark side of nuclear-mitochondrial communication. EMBO J. 2017;36:1123-1133.

    Not in our library10.15252/embj.201695546

  103. 103.

    Feeley K.P., Bray A.W., Westbrook D.G., Johnson L.W., Kesterson R.A., Ballinger S.W., Welch D.R. Mitochondrial Genetics Regulate Breast Cancer Tumorigenicity and Metastatic Potential. Cancer Res. 2015;75:4429-4436.

    Not in our library10.1158/0008-5472.can-15-0074

  104. 104.

    Brinker A.E., Vivian C.J., Koestler D.C., Tsue T.T., Jensen R.A., Welch D.R. Mitochondrial Haplotype Alters Mammary Cancer Tumorigenicity and Metastasis in an Oncogenic Driver-Dependent Manner. Cancer Res. 2017;77:6941-6949.

    Not in our library10.1158/0008-5472.can-17-2194

  105. 105.
    Optimized high-throughput microRNA expression profiling provides novel biomarker assessment of clinical prostate and breast cancer biopsies. · 2006
    No notice
  106. 106.

    Lu Z., Liu M., Stribinskis V., Klinge C.M., Ramos K.S., Colburn N.H., Li Y. MicroRNA-21 Promotes Cell Transformation by Targeting the Programmed Cell Death 4 Gene. Oncogene. 2008;27:4373-4379.

    Not in our library10.1038/onc.2008.72

  107. 107.

    Yan L.-X., Huang X.-F., Shao Q., Huang M.-Y., Deng L., Wu Q.-L., Zeng Y.-X., Shao J.-Y. MicroRNA miR-21 overexpression in human breast cancer is associated with advanced clinical stage, lymph node metastasis and patient poor prognosis. RNA. 2008;14:2348-2360.

    Not in our library10.1261/rna.1034808

  108. 108.

    Zhu S., Wu H., Wu F., Nie D., Sheng S., Mo Y.Y. MicroRNA-21 targets tumor suppressor genes in invasion and metastasis. Cell Res. 2008;18:350-359.

    Not in our library10.1038/cr.2008.24

  109. 109.

    Gong C., Yao Y., Wang Y., Liu B., Wu W., Chen J., Su F., Yao H., Song E. Up-regulation of miR-21 mediates resistance to trastuzumab therapy for breast cancer. J. Biol. Chem. 2011;286:19127-19137.

    Not in our library10.1074/jbc.m110.216887

  110. 110.

    Rask L., Balslev E.V.A., JØRgensen S., Eriksen J., Flyger H., MØLler S., HØGdall E., Litman T., Schnack Nielsen B. High expression of miR-21 in tumor stroma correlates with increased cancer cell proliferation in human breast cancer. APMIS. 2011;119:663-673.

    Not in our library10.1111/j.1600-0463.2011.02782.x

  111. 111.
    Knockdown of miR-21 in human breast cancer cell lines inhibits proliferation, in vitro migration and in vivotumor growth · 2011
    No notice
  112. 112.

    Han M., Wang Y., Liu M., Bi X., Bao J., Zeng N., Zhu Z., Mo Z., Wu C., Chen X. MiR-21 regulates EMT phenotype and HIF-1α expression in third–sphereforming breast cancer stem cell-like cells. Cancer Sci. 2012;103:1058-1064.

    Not in our library10.1111/j.1349-7006.2012.02281.x

  113. 113.

    Li S., Liang Z., Xu L., Zou F. MicroRNA-21: A ubiquitously expressed pro-survival factor in cancer and other diseases. Mol. Cell Biochem. 2012;360:147-158.

    Not in our library10.1007/s11010-011-1052-6

  114. 114.

    Petrović N., Mandušić V., Stanojević B., Lukić S., Todorović L., Roganović J., Dimitrijević B. The difference in miR-21 expression levels between invasive and non-invasive breast cancers emphasizes its role in breast cancer invasion. Med. Oncol. 2014;31:1-9.

    Not in our library10.1007/s12032-014-0867-x

  115. 115.

    Petrovic N. miR-21 Might be Involved in Breast Cancer Promotion and Invasion Rather than in Initial Events of Breast Cancer Development. Mol. Diagn. Ther. 2016;20:97-110.

    Not in our library10.1007/s40291-016-0186-3

  116. 116.

    Svoronos A.A., Engelman D.M., Slack F.J. OncomiR or Tumor Suppressor? The Duplicity of MicroRNAs in Cancer. Cancer Res. 2016;76:3666.

    Not in our library10.1158/0008-5472.can-16-0359

  117. 117.

    Klinge C.M. miRNAs and estrogen action. Trends Endocrinol. Metab. 2012;23:223-233.

    Not in our library10.1016/j.tem.2012.03.002

  118. 118.

    Zhang W., Xu J., Shi Y., Sun Q., Zhang Q., Guan X. The novel role of miRNAs for tamoxifen resistance in human breast cancer. Cell Mol. Life Sci. 2015;72:2575-2584.

    Not in our library10.1007/s00018-015-1887-1

  119. 119.

    Hsu S.-D., Tseng Y.-T., Shrestha S., Lin Y.-L., Khaleel A., Chou C.-H., Chu C.-F., Huang H.-Y., Lin C.-M., Ho S.-Y., et al. miRTarBase update 2014: An information resource for experimentally validated miRNA-target interactions. Nucleic Acids Res. 2014;42:D78-D85.

    Not in our library10.1093/nar/gkt1266

  120. 120.

    Liu S., Zhang P., Chen Z., Liu M., Li X., Tang H. MicroRNA-7 downregulates XIAP expression to suppress cell growth and promote apoptosis in cervical cancer cells. FEBS Lett. 2013;587:2247-2253.

    Not in our library10.1016/j.febslet.2013.05.054

  121. 121.

    Zhang X., Zhang X., Hu S., Zheng M., Zhang J., Zhao J., Zhang X., Yan B., Jia L., Zhao J., et al. Identification of miRNA-7 by genome-wide analysis as a critical sensitizer for TRAIL-induced apoptosis in glioblastoma cells. Nucleic Acids Res. 2017;45:5930-5944.

    Not in our library10.1093/nar/gkx317

  122. 122.
    Expression of microRNA and their gene targets are dysregulated in preinvasive breast cancer · 2011
    No notice
  123. 123.

    Cui Y.-X., Bradbury R., Flamini V., Wu B., Jordan N., Jiang W.G. MicroRNA-7 suppresses the homing and migration potential of human endothelial cells to highly metastatic human breast cancer cells. Br. J. Cancer. 2017;117:89.

    Not in our library10.1038/bjc.2017.156

  124. 124.

    Liu Y., Zhang Y., Wu H., Li Y., Zhang Y., Liu M., Li X., Tang H. miR-10a suppresses colorectal cancer metastasis by modulating the epithelial-to-mesenchymal transition and anoikis. Cell Death Dis. 2017;8:e2739.

    Not in our library10.1038/cddis.2017.61

  125. 125.

    Fan Q., Meng X., Liang H., Zhang H., Liu X., Li L., Li W., Sun W., Zhang H., Zen K., et al. miR-10a inhibits cell proliferation and promotes cell apoptosis by targeting BCL6 in diffuse large B-cell lymphoma. Protein Cell. 2016;7:899-912.

    Not in our library10.1007/s13238-016-0316-z

  126. 126.

    Long M.-J., Wu F.-X., Li P., Liu M., Li X., Tang H. MicroRNA-10a targets CHL1 and promotes cell growth, migration and invasion in human cervical cancer cells. Cancer Lett. 2012;324:186-196.

    Not in our library10.1016/j.canlet.2012.05.022

  127. 127.

    Foley N.H., Bray I., Watters K.M., Das S., Bryan K., Bernas T., Prehn J.H.M., Stallings R.L. MicroRNAs 10a and 10b are potent inducers of neuroblastoma cell differentiation through targeting of nuclear receptor corepressor 2. Cell Death Differ. 2011;18:1089-1098.

    Not in our library10.1038/cdd.2010.172

  128. 128.

    Arai T., Okato A., Kojima S., Idichi T., Koshizuka K., Kurozumi A., Kato M., Yamazaki K., Ishida Y., Naya Y., et al. Regulation of spindle and kinetochore-associated protein 1 by antitumor miR-10a-5p in renal cell carcinoma. Cancer Sci. 2017;108:2088-2101.

    Not in our library10.1111/cas.13331

  129. 129.

    Hudson J., Duncavage E., Tamburrino A., Salerno P., Xi L., Raffeld M., Moley J., Chernock R.D. Overexpression of miR-10a and miR-375 and downregulation of YAP1 in medullary thyroid carcinoma. Exp. Mol. Pathol. 2013;95:62-67.

    Not in our library10.1016/j.yexmp.2013.05.001

  130. 130.

    Wang Y., Liu Z., Yao B., Dou C., Xu M., Xue Y., Ding L., Jia Y., Zhang H., Li Q., et al. Long non–coding RNA TUSC7 acts a molecular sponge for miR-10a and suppresses EMT in hepatocellular carcinoma. Tumour Biol. 2016;37:11429-11441.

    Not in our library10.1007/s13277-016-4892-6

  131. 131.

    Liu Y., Xu N., Liu B., Huang Y., Zeng H., Yang Z., He Z., Guo H. Long noncoding RNA RP11-838N2.4 enhances the cytotoxic effects of temozolomide by inhibiting the functions of miR-10a in glioblastoma cell lines. Oncotarget. 2016;7:43835-43851.

    Not in our library10.18632/oncotarget.9699

  132. 132.

    Ke K., Lou T. MicroRNA-10a suppresses breast cancer progression via PI3K/Akt/mTOR pathway. Oncol. Lett. 2017;14:5994-6000.

    Not in our library10.3892/ol.2017.6930

  133. 133.

    Hoppe R., Achinger-Kawecka J., Winter S., Fritz P., Lo W.-Y., Schroth W., Brauch H. Increased expression of miR-126 and miR-10a predict prolonged relapse-free time of primary oestrogen receptor-positive breast cancer following tamoxifen treatment. Eur. J. Cancer. 2013;49:3598-3608.

    Not in our library10.1016/j.ejca.2013.07.145

  134. 134.

    Kim C., Go E.J., Kim A. Recurrence prediction using microRNA expression in hormone receptor positive breast cancer during tamoxifen treatment. Biomarkers. 2018;23:804-811.

    Not in our library10.1080/1354750x.2018.1499131

  135. 135.

    Castellano L., Giamas G., Jacob J., Coombes R.C., Lucchesi W., Thiruchelvam P., Barton G., Jiao L.R., Wait R., Waxman J., et al. The estrogen receptor-alpha induced microRNA signature regulates itself and its transcriptional response. Proc. Natl. Acad. Sci. USA. 2009;106:15732-15737.

    Not in our library10.1073/pnas.0906947106

  136. 136.

    Zhang N., Zhang H., Liu Y., Su P., Zhang J., Wang X., Sun M., Chen B., Zhao W., Wang L., et al. SREBP1, targeted by miR-18a-5p, modulates epithelial–mesenchymal transition in breast cancer via forming a co-repressor complex with Snail and HDAC1/2. Cell Death Differ. 2018.

    Not in our library10.1038/s41418-018-0158-8

  137. 137.

    Li X., Wu Y., Liu A., Tang X. Long non-coding RNA UCA1 enhances tamoxifen resistance in breast cancer cells through a miR-18a-HIF1alpha feedback regulatory loop. Tumor Biol. 2016;37:14733-14743.

    Not in our library10.1007/s13277-016-5348-8

  138. 138.

    Yoshimoto N., Toyama T., Takahashi S., Sugiura H., Endo Y., Iwasa M., Fujii Y., Yamashita H. Distinct expressions of microRNAs that directly target estrogen receptor α in human breast cancer. Breast Cancer Res. Treat. 2011;130:331-339.

    Not in our library10.1007/s10549-011-1672-2

  139. 139.

    Wickramasinghe N., Manavalan T., Dougherty S., Riggs K., Li Y., Klinge C. Estradiol downregulates miR-21 expression and increases miR-21 target gene expression in MCF-7 breast cancer cells. Nucleic Acids Res. 2009;37:2584-2595.

    Not in our library10.1093/nar/gkp117

  140. 140.

    Queiros A.M., Eschen C., Fliegner D., Kararigas G., Dworatzek E., Westphal C., Sanchez Ruderisch H., Regitz-Zagrosek V. Sex- and estrogen-dependent regulation of a miRNA network in the healthy and hypertrophied heart. Int. J. Cardiol. 2013;169:331-338.

    Not in our library10.1016/j.ijcard.2013.09.002

  141. 141.

    Kanwal R., Plaga A.R., Liu X., Shukla G.C., Gupta S. MicroRNAs in prostate cancer: Functional role as biomarkers. Cancer Lett. 2017;407:9-20.

    Not in our library10.1016/j.canlet.2017.08.011

  142. 142.

    Li S., Yang X., Yang J., Zhen J., Zhang D. Serum microRNA-21 as a potential diagnostic biomarker for breast cancer: A systematic review and meta-analysis. Clin. Exp. Med. 2016;16:29-35.

    Not in our library10.1007/s10238-014-0332-3

  143. 143.

    Chen L., Zheng J., Zhang Y., Yang L., Wang J., Ni J., Cui D., Yu C., Cai Z. Tumor-specific Expression of MicroRNA-26a Suppresses Human Hepatocellular Carcinoma Growth via Cyclin-dependent and-independent Pathways. Mol. Ther. 2011;19:1521-1528.

    Not in our library10.1038/mt.2011.64

  144. 144.

    Tan S., Ding K., Li R., Zhang W., Li G., Kong X., Qian P., Lobie P.E., Zhu T. Identification of miR-26 as a key mediator of estrogen stimulated cell proliferation by targeting CHD1, GREB1 and KPNA2. Breast Cancer Res. 2014;16:R40.

    Not in our library10.1186/bcr3644

  145. 145.

    Jansen M.P., Reijm E.A., Sieuwerts A.M., Ruigrok-Ritstier K., Look M.P., Rodriguez-Gonzalez F.G., Heine A.A., Martens J.W., Sleijfer S., Foekens J.A., et al. High miR-26a and low CDC2 levels associate with decreased EZH2 expression and with favorable outcome on tamoxifen in metastatic breast cancer. Breast Cancer Res. Treat. 2012;133:937-947.

    Not in our library10.1007/s10549-011-1877-4

  146. 146.

    Tanno T., Zhang P., Lazarski C.A., Liu Y., Zheng P. An aptamer–based targeted delivery of miR-26a protects mice against chemotherapy toxicity while suppressing tumor growth. Blood Adv. 2017;1:1107-1119.

    Not in our library10.1182/bloodadvances.2017004705

  147. 147.

    Muluhngwi P., Krishna A., Vittitow S.L., Napier J.T., Richardson K.M., Ellis M., Mott J.L., Klinge C.M. Tamoxifen differentially regulates miR-29b-1 and miR-29a expression depending on endocrine–sensitivity in breast cancer cells. Cancer Lett. 2017;388:230-238.

    Not in our library10.1016/j.canlet.2016.12.007

  148. 148.

    Ding D., Li C., Zhao T., Li D., Yang L., Zhang B. LncRNA H19/miR-29b-3p/PGRN Axis Promoted Epithelial-Mesenchymal Transition of Colorectal Cancer Cells by Acting on Wnt Signaling. Mol. Cells. 2018;41:423-435.

    Not in our library10.14348/molcells.2018.2258

  149. 149.

    Zhang X., Cheng L., Xu L., Zhang Y., Yang Y., Fu Q., Mi W., Li H. The lncRNA H19 mediates the protective eEffect of hypoxia postconditioning against hypoxia-Rreoxygenation injury to senescent cardiomyocytes by targeting microRNA-29b-3p. Shock. 2018.

    Not in our library10.1097/shk.0000000000001213

  150. 150.

    Zhang H., Li H., Ge A., Guo E., Liu S., Zhang L. Long non-coding RNA TUG1 inhibits apoptosis and inflammatory response in LPS-treated H9c2 cells by down-regulation of miR–29b. Biomed. Pharmacother. 2018;101:663-669.

    Not in our library10.1016/j.biopha.2018.02.129

  151. 151.

    Du P., Zhao H., Peng R., Liu Q., Yuan J., Peng G., Liao Y. LncRNA-XIST interacts with miR-29c to modulate the chemoresistance of glioma cell to TMZ through DNA mismatch repair pathway. Biosci. Rep. 2017;37:BSR20170696.

    Not in our library10.1042/bsr20170696

  152. 152.

    Han Q., Li L., Liang H., Li Y., Xie J., Wang Z. Downregulation of lncRNA X Inactive Specific Transcript (XIST) Suppresses Cell Proliferation and Enhances Radiosensitivity by Upregulating mir-29c in Nasopharyngeal Carcinoma Cells. Med. Sci. Monit. 2017;23:4798-4807.

    Not in our library10.12659/msm.905370

  153. 153.

    Alipoor F.J., Asadi M.H., Torkzadeh-Mahani M. MIAT lncRNA is overexpressed in breast cancer and its inhibition triggers senescence and G1 arrest in MCF7 cell line. J. Cell Biochem. 2018;119:6470-6481.

    Not in our library10.1002/jcb.26678

  154. 154.

    Jiang H., Zhang G., Wu J.H., Jiang C.P. Diverse roles of miR-29 in cancer (review). Oncol. Rep. 2014;31:1509-1516.

    Not in our library10.3892/or.2014.3036

  155. 155.

    Bhat-Nakshatri P., Wang G., Collins N.R., Thomson M.J., Geistlinger T.R., Carroll J.S., Brown M., Hammond S., Srour E.F., Liu Y., et al. Estradiol-regulated microRNAs control estradiol response in breast cancer cells. Nucleic Acids Res. 2009;37:4850-4861.

    Not in our library10.1093/nar/gkp500

  156. 156.

    Ling X.H., Chen Z.Y., Luo H.W., Liu Z.Z., Liang Y.K., Chen G.X., Jiang F.N., Zhong W.D. BCL9, a coactivator for Wnt/beta-catenin transcription, is targeted by miR-30c and is associated with prostate cancer progression. Oncol. Lett. 2016;11:2001-2008.

    Not in our library10.3892/ol.2016.4161

  157. 157.

    Ni L.Y., Zhao J.D., Lu Y.H., Li W., Li B.L., Wang X.C., Meng Q.G. MicroRNA-30c suppressed giant-cell tumor of bone cell metastasis and growth via targeting HOXA1. Eur. Rev. Med. Pharmacol. Sci. 2017;21:4819-4827.

    Not in our library

  158. 158.

    Huang Y.Q., Ling X.H., Yuan R.Q., Chen Z.Y., Yang S.B., Huang H.X., Zhong W.D., Qiu S.P. miR-30c suppresses prostate cancer survival by targeting the ASF/SF2 splicing factor oncoprotein. Mol. Med. Rep. 2017;16:2431-2438.

    Not in our library10.3892/mmr.2017.6910

  159. 159.

    Zhang J., Wang X., Wang Y., Peng R., Lin Z., Wang Y., Hu B., Wang J., Shi G. Low expression of microRNA-30c promotes prostate cancer cells invasion involved in downregulation of KRAS protein. Oncol. Lett. 2017;14:363-368.

    Not in our library10.3892/ol.2017.6163

  160. 160.

    Su W., Hong L., Xu X., Huang S., Herpai D., Li L., Xu Y., Truong L., Hu W.-Y., Wu X., et al. miR-30 disrupts senescence and promotes cancer by targeting both p16INK4A and DNA damage pathways. Oncogene. 2018;37:5618-5632.

    Not in our library10.1038/s41388-018-0358-1

  161. 161.

    Liang T., Zhou B., Shi L., Wang H., Chu Q., Xu F., Li Y., Chen R., Shen C., Schinckel AP. lncRNA AK017368 promotes proliferation and suppresses differentiation of myoblasts in skeletal muscle development by attenuating the function of miR-30c. FASEB J. 2017;32:377-389.

    Not in our library10.1096/fj.201700560rr

  162. 162.

    Liu X., Li M., Peng Y., Hu X., Xu J., Zhu S., Yu Z., Han S. miR-30c regulates proliferation, apoptosis and differentiation via the Shh signaling pathway in P19 cells. Exp. Mol. Med. 2016;48:e248.

    Not in our library10.1038/emm.2016.57

  163. 163.

    Croset M., Pantano F., Kan C.W.S., Bonnelye E., Descotes F., Alix-Panabières C., Lecellier C.-H., Bachelier R., Allioli N., Hong S.-S., et al. MicroRNA-30 family members inhibit breast cancer invasion, osteomimicry, and bone destruction by directly targeting multiple bone metastasis-associated genes. Cancer Res. 2018;78:5259-5273.

    Not in our library10.1158/0008-5472.can-17-3058

  164. 164.

    Razaviyan J., Hadavi R., Tavakoli R., Kamani F., Paknejad M., Mohammadi-Yeganeh S. Expression of miRNAs Targeting mTOR and S6K1 Genes of mTOR Signaling Pathway Including miR-96, miR-557, and miR-3182 in Triple-Negative Breast Cancer. Appl. Biochem. Biotechnol. 2018;186:1074-1089.

    Not in our library10.1007/s12010-018-2773-8

  165. 165.

    Cai T., Long J., Wang H., Liu W., Zhang Y. Identification and characterization of miR-96, a potential biomarker of NSCLC, through bioinformatic analysis. Oncol. Rep. 2017;38:1213-1223.

    Not in our library10.3892/or.2017.5754

  166. 166.

    Xiong D.D., Lv J., Wei K.L., Feng Z.B., Chen J.T., Liu K.C., Chen G., Luo D.Z. A nine–miRNA signature as a potential diagnostic marker for breast carcinoma: An integrated study of 1110 cases. Oncol. Rep. 2017;37:3297-3304.

    Not in our library10.3892/or.2017.5600

  167. 167.

    Scott G.K., Goga A., Bhaumik D., Berger C.E., Sullivan C.S., Benz C.C. Coordinate Suppression of ERBB2 and ERBB3 by Enforced Expression of Micro-RNA miR-125a or miR-125b. J. Biol. Chem. 2007;282:1479-1486.

    Not in our library10.1074/jbc.m609383200

  168. 168.

    Zhang Y., Yan L.-X., Wu Q.-N., Du Z.-M., Chen J., Liao D.-Z., Huang M.-Y., Hou J.-H., Wu Q.-L., Zeng M.-S., et al. miR-125b Is Methylated and Functions as a Tumor Suppressor by Regulating the ETS1 Proto–oncogene in Human Invasive Breast Cancer. Cancer Res. 2011;71:3552-3562.

    Not in our library10.1158/0008-5472.can-10-2435

  169. 169.

    Vilquin P., Donini C.F., Villedieu M., Grisard E., Corbo L., Bachelot T., Vendrell J.A., Cohen P.A. MicroRNA-125b upregulation confers aromatase inhibitor resistance and is a novel marker of poor prognosis in breast cancer. Breast Cancer Res. 2015;17:13.

    Not in our library10.1186/s13058-015-0515-1

  170. 170.

    Matamala N., Vargas M.T., González-Cámpora R., Miñambres R., Arias J.I., Menéndez P., Andrés-León E., Gómez-López G., Yanowsky K., Calvete-Candenas J., et al. Tumor MicroRNA Expression Profiling Identifies Circulating MicroRNAs for Early Breast Cancer Detection. Clin. Chem. 2015;61:1098.

    Not in our library10.1373/clinchem.2015.238691

  171. 171.

    Shivapurkar N., Vietsch E.E., Carney E., Isaacs C., Wellstein A. Circulating microRNAs in patients with hormone receptor-positive, metastatic breast cancer treated with dovitinib. Clin. Trans. Med. 2017;6:37.

    Not in our library10.1186/s40169-017-0169-y

  172. 172.

    Hoppe R., Fan P., Buttner F., Winter S., Tyagi A.K., Cunliffe H., Jordan V.C., Brauch H. Profiles of miRNAs matched to biology in aromatase inhibitor resistant breast cancer. Oncotarget. 2016;7:71235-71254.

    Not in our library10.18632/oncotarget.12103

  173. 173.

    Pan J.-Y., Zhang F., Sun C.-C., Li S.-J., Li G., Gong F.-Y., Bo T., He J., Hua R.-X., Hu W.-D., et al. miR-134: A Human Cancer Suppressor? Mol. Ther. Nucleic Acids. 2017;6:140-149.

    Not in our library10.1016/j.omtn.2016.11.003

  174. 174.
    The forkhead transcription factor FOXM1 promotes endocrine resistance and invasiveness in estrogen receptor-positive breast cancer by expansion of stem-like cancer cells · 2014
    No notice
  175. 175.
    microRNA expression profiling on individual breast cancer patients identifies novel panel of circulating microRNA for early detection · 2016
    No notice
  176. 176.

    Benetatos L., Hatzimichael E., Londin E., Vartholomatos G., Loher P., Rigoutsos I., Briasoulis E. The microRNAs within the DLK1-DIO3 genomic region: Involvement in disease pathogenesis. Cell Mol. Life Sci. 2013;70:795-814.

    Not in our library10.1007/s00018-012-1080-8

  177. 177.

    Millour J., Constantinidou D., Stavropoulou A.V., Wilson M.S.C., Myatt S.S., Kwok J.M.M., Sivanandan K., Coombes R.C., Medema R.H., Hartman J., et al. FOXM1 is a transcriptional target of ER[alpha] and has a critical role in breast cancer endocrine sensitivity and resistance. Oncogene. 2010;29:2983-2995.

    Not in our library10.1038/onc.2010.47

  178. 178.

    Dinami R., Ercolani C., Petti E., Piazza S., Ciani Y., Sestito R., Sacconi A., Biagioni F., le Sage C., Agami R., et al. miR-155 drives telomere fragility in human breast cancer by targeting TRF1. Cancer Res. 2014;74:4145-4156.

    Not in our library10.1158/0008-5472.can-13-2038

  179. 179.

    Zhang C.M., Zhao J., Deng H.Y. miR-155 promotes proliferation of human breast cancer MCF-7 cells through targeting tumor protein 53–induced nuclear protein 1. J. Biomed. Sci. 2013;20:79.

    Not in our library10.1186/1423-0127-20-79

  180. 180.

    Brown C.Y., Dayan S., Wong S.W., Kaczmarek A., Hope C.M., Pederson S.M., Arnet V., Goodall G.J., Russell D., Sadlon T.J. FOXP3 and miR-155 cooperate to control the invasive potential of human breast cancer cells by down regulating ZEB2 independently of ZEB1. Oncotarget. 2018;9:27708-27727.

    Not in our library10.18632/oncotarget.25523

  181. 181.

    Zhou X., Ye F., Yin C., Zhuang Y., Yue G., Zhang G. The Interaction Between miR-141 and lncRNA-H19 in Regulating Cell Proliferation and Migration in Gastric Cancer. Cell Physiol. Biochem. 2015;36:1440-1452.

    Not in our library10.1159/000430309

  182. 182.

    Chen L., Wang W., Cao L., Li Z., Wang X. Long Non-Coding RNA CCAT1 Acts as a Competing Endogenous RNA to Regulate Cell Growth and Differentiation in Acute Myeloid Leukemia. Mol. Cells. 2016;39:330-336.

    Not in our library10.14348/molcells.2016.2308

  183. 183.

    Cao S., Wang Y., Li J., Lv M., Niu H., Tian Y. Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function. Am. J. Cancer Res. 2016;6:2561-2574.

    Not in our library

  184. 184.

    Luan T., Zhang X., Wang S., Song Y., Zhou S., Lin J., An W., Yuan W., Yang Y., Cai H., et al. Long non–coding RNA MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p. Oncotarget. 2017;8:76153-76164.

    Not in our library10.18632/oncotarget.19190

  185. 185.

    Dou L., Lin H., Wang K., Zhu G., Zou X., Chang E., Zhu Y. Long non-coding RNA CCAT1 modulates neuropathic pain progression through sponging miR-155. Oncotarget. 2017;8:89949-89957.

    Not in our library10.18632/oncotarget.21192

  186. 186.

    Eichelser C., Flesch-Janys D., Chang-Claude J., Pantel K., Schwarzenbach H. Deregulated Serum Concentrations of Circulating Cell–Free MicroRNAs miR-17, miR-34a, miR-155, and miR-373 in Human Breast Cancer Development and Progression. Clin. Chem. 2013;59:1489-1496.

    Not in our library10.1373/clinchem.2013.205161

  187. 187.

    Liu J., Shi W., Wu C., Ju J., Jiang J. miR-181b as a key regulator of the oncogenic process and its clinical implications in cancer (Review). Biomed. Rep. 2014;2:7-11.

    Not in our library10.3892/br.2013.199

  188. 188.

    Cui B., Li B., Liu Q., Cui Y. lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR-181b. J. Cell Biochem. 2017;118:4548-4557.

    Not in our library10.1002/jcb.26116

  189. 189.
    Oncogenic MicroRNAs: miR-155, miR-19a, miR-181b, and miR-24 enable monitoring of early breast cancer in serum · 2014
    No notice
  190. 190.

    Yoo J.-O., Kwak S.-Y., An H.-J., Bae I.-H., Park M.-J., Han Y.-H. miR-181b-3p promotes epithelial–mesenchymal transition in breast cancer cells through Snail stabilization by directly targeting YWHAG. Biochim. Biophys. Acta Mol. Cell Res. 2016;1863:1601-1611.

    Not in our library10.1016/j.bbamcr.2016.04.016

  191. 191.

    Wang R., Tian S., Wang H.B., Chu D.P., Cao J.L., Xia H.F., Ma X. MiR-185 is involved in human breast carcinogenesis by targeting Vegfa. FEBS Lett. 2014;588:4438-4447.

    Not in our library10.1016/j.febslet.2014.09.045

  192. 192.

    Tang H., Liu P., Yang L., Xie X., Ye F., Wu M., Liu X., Chen B., Zhang L., Xie X. miR-185 Suppresses Tumor Proliferation by Directly Targeting E2F6 and DNMT1 and Indirectly Upregulating BRCA1 in Triple–Negative Breast Cancer. Mol. Cancer Ther. 2014;13:3185.

    Not in our library10.1158/1535-7163.mct-14-0243

  193. 193.

    Zou Q., Wu H., Fu F., Yi W., Pei L., Zhou M. RKIP suppresses the proliferation and metastasis of breast cancer cell lines through up–regulation of miR-185 targeting HMGA2. Arch. Biochem. Biophys. 2016;610:25-32.

    Not in our library10.1016/j.abb.2016.09.007

  194. 194.

    Imam J.S., Buddavarapu K., Lee-Chang J.S., Ganapathy S., Camosy C., Chen Y., Rao M.K. MicroRNA-185 suppresses tumor growth and progression by targeting the Six1 oncogene in human cancers. Oncogene. 2010;29:4971-4979.

    Not in our library10.1038/onc.2010.233

  195. 195.
    MiR-193b regulates breast cancer cell migration and vasculogenic mimicry by targeting dimethylarginine dimethylaminohydrolase 1 · 2017
    Not checked
  196. 196.

    Xie F., Hosany S., Zhong S., Jiang Y., Zhang F., Lin L., Wang X., Gao S., Hu X. MicroRNA-193a inhibits breast cancer proliferation and metastasis by downregulating WT1. PLoS ONE. 2017;12:e0185565.

    Not in our library10.1371/journal.pone.0185565

  197. 197.

    Tsai K.-W., Leung C.-M., Lo Y.-H., Chen T.-W., Chan W.-C., Yu S.-Y., Tu Y.-T., Lam H.-C., Li S.-C., Ger L.-P., et al. Arm Selection Preference of MicroRNA–193a Varies in Breast Cancer. Sci. Rep. 2016;6:28176.

    Not in our library10.1038/srep28176

  198. 198.

    Dvinge H., Git A., Graf S., Salmon-Divon M., Curtis C., Sottoriva A., Zhao Y., Hirst M., Armisen J., Miska E.A., et al. The shaping and functional consequences of the microRNA landscape in breast cancer. Nature. 2013;497:378-382.

    Not in our library10.1038/nature12108

  199. 199.

    Chen Z., Li Y., Zhang H., Huang P., Luthra R. Hypoxia–regulated microRNA-210 modulates mitochondrial function and decreases ISCU and COX10 expression. Oncogene. 2010;29:4362-4368.

    Not in our library10.1038/onc.2010.193

  200. 200.

    Fasanaro P., D’Alessandra Y., Di Stefano V., Melchionna R., Romani S., Pompilio G., Capogrossi M.C., Martelli F. MicroRNA-210 Modulates Endothelial Cell Response to Hypoxia and Inhibits the Receptor Tyrosine Kinase Ligand Ephrin–A3. J. Biol. Chem. 2008;283:15878-15883.

    Not in our library10.1074/jbc.m800731200

  201. 201.
    Global MicroRNA Expression Profiling Identifies MiR-210 Associated with Tumor Proliferation, Invasion and Poor Clinical Outcome in Breast Cancer · 2011
    No notice
  202. 202.

    Camps C., Buffa F.M., Colella S., Moore J., Sotiriou C., Sheldon H., Harris A.L., Gleadle J.M., Ragoussis J. has-miR-210 Is Induced by Hypoxia and Is an Independent Prognostic Factor in Breast Cancer. Clin. Cancer Res. 2008;14:1340-1348.

    Not in our library10.1158/1078-0432.ccr-07-1755

  203. 203.

    Zhao J.-J., Lin J., Yang H., Kong W., He L., Ma X., Coppola D., Cheng J.Q. MicroRNA-221/222 negatively regulates ERalpha and associates with tamoxifen resistance in breast cancer. J. Biol. Chem. 2008;283:31079-31086.

    Not in our library10.1074/jbc.m806041200

  204. 204.

    Di Leva G., Gasparini P., Piovan C., Ngankeu A., Garofalo M., Taccioli C., Iorio M.V., Li M., Volinia S., Alder H., et al. MicroRNA Cluster 221–222 and Estrogen Receptor {alpha} Interactions in Breast Cancer. J. Natl. Cancer Inst. 2010;102:706-721.

    Not in our library10.1093/jnci/djq102

  205. 205.
    Estrogen Mediated-Activation of miR-191/425 Cluster Modulates Tumorigenicity of Breast Cancer Cells Depending on Estrogen Receptor Status · 2013
    Corrected
  206. 206.

    Rao X., Di Leva G., Li M., Fang F., Devlin C., Hartman-Frey C., Burow M.E., Ivan M., Croce C.M., Nephew K.P. MicroRNA-221/222 confers breast cancer fulvestrant resistance by regulating multiple signaling pathways. Oncogene. 2011;30:1082-1097.

    Not in our library10.1038/onc.2010.487

  207. 207.

    Miller T.E., Ghoshal K., Ramaswamy B., Roy S., Datta J., Shapiro C.L., Jacob S., Majumder S. MicroRNA-221/222 confers tamoxifen resistance in breast cancer by targeting p27(Kip1). J. Biol. Chem. 2008;283:29897-29903.

    Not in our library10.1074/jbc.m804612200

  208. 208.

    Lu Y., Roy S., Nuovo G., Ramaswamy B., Miller T., Shapiro C., Jacob S.T., Majumder S. Anti-microRNA-222 (Anti-miR-222) and –181B Suppress Growth of Tamoxifen–resistant Xenografts in Mouse by Targeting TIMP3 Protein and Modulating Mitogenic Signal. J. Biol. Chem. 2011;286:42292-42302.

    Not in our library10.1074/jbc.m111.270926

  209. 209.

    Dentelli P., Rosso A., Orso F., Olgasi C., Taverna D., Brizzi M.F. microRNA-222 controls neovascularization by regulating signal transducer and activator of transcription 5A expression. Arterioscler. Thromb. Vasc. Biol. 2010;30:1562-1568.

    Not in our library10.1161/atvbaha.110.206201

  210. 210.

    Zhang Y., Lin X., Zhang L., Hong W., Zeng K. MicroRNA-222 regulates the viability of fibroblasts in hypertrophic scars via matrix metalloproteinase 1. Exp. Ther. Med. 2018;15:1803-1808.

    Not in our library10.3892/etm.2017.5634

  211. 211.

    Li Y., Liang C., Ma H., Zhao Q., Lu Y., Xiang Z., Li L., Qin J., Chen Y., Cho W.C., et al. miR-221/222 promotes S–phase entry and cellular migration in control of basal–like breast cancer. Molecules. 2014;19:7122-7137.

    Not in our library10.3390/molecules19067122

  212. 212.

    Wu Q., Lu Z., Li H., Lu J., Guo L., Ge Q. Next–generation sequencing of microRNAs for breast cancer detection. J. Biomed. Biotechnol. 2011;2011:597145.

    Not in our library10.1155/2011/597145

  213. 213.

    Ferretti E., De Smaele E., Miele E., Laneve P., Po A., Pelloni M., Paganelli A., Di Marcotullio L., Caffarelli E., Screpanti I., et al. Concerted microRNA control of Hedgehog signalling in cerebellar neuronal progenitor and tumour cells. EMBO J. 2008;27:2616-2627.

    Not in our library10.1038/emboj.2008.172

  214. 214.

    Kuo W.-T., Yu S.-Y., Li S.-C., Lam H.-C., Chang H.-T., Chen W.-S., Yeh C.-Y., Hung S.-F., Liu T.-C., Wu T., et al. MicroRNA-324 in Human Cancer: miR-324-5p and miR-324-3p Have Distinct Biological Functions in Human Cancer. Anticancer. Res. 2016;36:5189-5196.

    Not in our library10.21873/anticanres.11089

  215. 215.

    Nie J., Liu L., Zheng W., Chen L., Wu X., Xu Y., Du X., Han W. microRNA-365, down-regulated in colon cancer, inhibits cell cycle progression and promotes apoptosis of colon cancer cells by probably targeting Cyclin D1 and Bcl-2. Carcinogenesis. 2012;33:220-225.

    Not in our library10.1093/carcin/bgr245

  216. 216.

    Hamada S., Masamune A., Miura S., Satoh K., Shimosegawa T. MiR-365 induces gemcitabine resistance in pancreatic cancer cells by targeting the adaptor protein SHC1 and pro–apoptotic regulator BAX. Cell Signal. 2014;26:179-185.

    Not in our library10.1016/j.cellsig.2013.11.003

  217. 217.

    Madhavan D., Peng C., Wallwiener M., Zucknick M., Nees J., Schott S., Rudolph A., Riethdorf S., Trumpp A., Pantel K., et al. Circulating miRNAs with prognostic value in metastatic breast cancer and for early detection of metastasis. Carcinogenesis. 2016;37:461-470.

    Not in our library10.1093/carcin/bgw008

  218. 218.

    Ward A., Shukla K., Balwierz A., Soons Z., König R., Sahin Ö., Wiemann S. microRNA-519a is a novel oncomir conferring tamoxifen resistance by targeting a network of tumor-suppressor genes in ER+ breast cancer. J. Pathol. 2014;233:368-379.

    Not in our library10.1002/path.4363

  219. 219.

    Breunig C., Pahl J., Kublbeck M., Miller M., Antonelli D., Erdem N., Wirth C., Will R., Bott A., Cerwenka A., et al. MicroRNA-519a-3p mediates apoptosis resistance in breast cancer cells and their escape from recognition by natural killer cells. Cell Death Dis. 2017;8:e2973.

    Not in our library10.1038/cddis.2017.364

  220. 220.

    Yahya S.M.M., Elsayed G.H. A summary for molecular regulations of miRNAs in breast cancer. Clin. Biochem. 2015;48:388-396.

    Not in our library10.1016/j.clinbiochem.2014.12.013

  221. 221.

    Zare M., Bastami M., Solali S., Alivand M.R. Aberrant miRNA promoter methylation and EMT–involving miRNAs in breast cancer metastasis: Diagnosis and therapeutic implications. J. Cell. Physiol. 2017;233:3729-3744.

    Not in our library10.1002/jcp.26116

  222. 222.

    Weidle U.H., Dickopf S., Hintermair C., Kollmorgen G., Birzele F., Brinkmann U. The Role of micro RNAs in Breast Cancer Metastasis: Preclinical Validation and Potential Therapeutic Targets. Cancer Genom. Proteom. 2018;15:17-39.

    Not in our library10.21873/cgp.20062

  223. 223.
    Exosomal miRNAs and miRNA dysregulation in cancer-associated fibroblasts · 2017
    No notice
  224. 224.

    Yau C., Meyer L., Benz S., Vaske C., Scott G., Egan B., Labhart P., Pourmand N., Benz C.C. FOXM1 cistrome predicts breast cancer metastatic outcome better than FOXM1 expression levels or tumor proliferation index. Breast Cancer Res. Treat. 2015;154:23-32.

    Not in our library10.1007/s10549-015-3589-7

  225. 225.

    Yuan B., Liu Y., Yu X., Yin L., Peng Y., Gao Y., Zhu Q., Cao T., Yang Y., Fan X., et al. FOXM1 contributes to taxane resistance by regulating UHRF1-controlled cancer cell stemness. Cell Death Dis. 2018;9:562.

    Not in our library10.1038/s41419-018-0631-9

  226. 226.
    MicroRNA-99 Family Targets AKT/mTOR Signaling Pathway in Dermal Wound Healing · 2013
    No notice
  227. 227.

    Wang X., Li Y., Qi W., Zhang N., Sun M., Huo Q., Cai C., Lv S., Yang Q. MicroRNA-99a inhibits tumor aggressive phenotypes through regulating HOXA1 in breast cancer cells. Oncotarget. 2015;6:32737-32747.

    Not in our library10.18632/oncotarget.5355

  228. 228.

    Turcatel G., Rubin N., El-Hashash A., Warburton D. MIR-99a and MIR-99b Modulate TGF-β Induced Epithelial to Mesenchymal Plasticity in Normal Murine Mammary Gland Cells. PLoS ONE. 2012;7:e31032.

    Not in our library10.1371/journal.pone.0031032

  229. 229.

    Yang Z., Han Y., Cheng K., Zhang G., Wang X. miR-99a directly targets the mTOR signalling pathway in breast cancer side population cells. Cell Prolif. 2014;47:587-595.

    Not in our library10.1111/cpr.12146

  230. 230.

    Haakensen V.D., Nygaard V., Greger L., Aure M.R., Fromm B., Bukholm I.R., Luders T., Chin S.F., Git A., Caldas C., et al. Subtype-specific microRNA expression signatures in breast cancer progression. Int. J. Cancer. 2016;139:1117-1128.

    Not in our library10.1002/ijc.30142

  231. 231.

    Li J., Song Z.J., Wang Y.Y., Yin Y., Liu Y., Nan X. Low levels of serum miR-99a is a predictor of poor prognosis in breast cancer. Genet. Mol. Res. 2016;15:BSR20170696.

    Not in our library10.4238/gmr.15038338

  232. 232.

    Kim S.-W., Ramasamy K., Bouamar H., Lin A.-P., Jiang D., Aguiar R.C.T. MicroRNAs miR-125a and miR-125b constitutively activate the NF-κB pathway by targeting the tumor necrosis factor alpha-induced protein 3 (TNFAIP3, A20). Proc. Natl. Acad. Sci. USA. 2012;109:7865-7870.

    Not in our library10.1073/pnas.1200081109

  233. 233.

    Iorio M.V., Ferracin M., Liu C.-G., Veronese A., Spizzo R., Sabbioni S., Magri E., Pedriali M., Fabbri M., Campiglio M., et al. MicroRNA gene expression deregulation in human breast cancer. Cancer Res. 2005;65:7065-7070.

    Not in our library10.1158/0008-5472.can-05-1783

  234. 234.

    Leucci E., Onnis A., Cocco M., De Falco G., Imperatore F., Giuseppina A., Costanzo V., Cerino G., Mannucci S., Cantisani R., et al. B-cell differentiation in EBV-positive Burkitt lymphoma is impaired at posttranscriptional level by miRNA–altered expression. Int. J. Cancer. 2010;126:1316-1326.

    Not in our library10.1002/ijc.24655

  235. 235.

    Wang Y., Kong D. Knockdown of lncRNA MEG3 inhibits viability, migration, and invasion and promotes apoptosis by sponging miR-127 in osteosarcoma cell. J. Cell Biochem. 2018;119:669-679.

    Not in our library10.1002/jcb.26230

  236. 236.

    Yang Z., Zhang Y., Wang L. A feedback inhibition between miRNA-127 and TGFbeta/c-Jun cascade in HCC cell migration via MMP13. PLoS ONE. 2013;8:e65256.

    Not in our library10.1371/journal.pone.0065256

  237. 237.

    Pajic M., Froio D., Daly S., Doculara L., Millar E., Graham P.H., Drury A., Steinmann A., de Bock C.E., Boulghourjian A., et al. miR-139-5p modulates radiotherapy resistance in breast cancer by repressing multiple gene networks of DNA repair and ROS defense. Cancer Res. 2018;78:501-515.

    Not in our library10.1158/0008-5472.can-16-3105

  238. 238.

    Teng H., Wang P., Xue Y., Liu X., Ma J., Cai H., Xi Z., Li Z., Liu Y. Role of HCP5-miR-139-RUNX1 Feedback Loop in Regulating Malignant Behavior of Glioma Cells. Mol. Ther. 2016;24:1806-1822.

    Not in our library10.1038/mt.2016.103

  239. 239.

    Jiang C., Tong Z., Fang W.-L., Fu Q.-B., Gu Y.-J., Lv T.-T., Liu D.-M., Xue W., Lv J.-W. Microrna-139-5p inhibits epithelial–mesenchymal transition and fibrosis in post-menopausal women with interstitial cystitis by targeting LPAR4 via the PI3K/Akt signaling pathway. J. Cell Biochem. 2018;119:6429-6441.

    Not in our library10.1002/jcb.26610

  240. 240.

    Chang L., Zhang D., Shi H., Bian Y., Guo R. MiR-143 inhibits endometrial cancer cell proliferation and metastasis by targeting MAPK1. Oncotarget. 2017;8:84384-84395.

    Not in our library10.18632/oncotarget.21037

  241. 241.

    Zhang Q., Feng Y., Liu P., Yang J. MiR-143 inhibits cell proliferation and invasion by targeting DNMT3A in gastric cancer. Tumour. Biol. 2017;39.

    Not in our library10.1177/1010428317711312

  242. 242.

    Wang J.H., Wang X.W., Qu D., Sun J.W., Guo F.X., Lu D. Upregulation of microRNA-143 reverses drug resistance in human breast cancer cells via inhibition of cytokine–induced apoptosis inhibitor 1. Oncol. Lett. 2017;13:4695-4700.

    Not in our library10.3892/ol.2017.6078

  243. 243.

    Ma Z., Luo Y., Qiu M. miR-143 Induces the Apoptosis of Prostate Cancer LNCap Cells by Suppressing Bcl-2 Expression. Med. Sci. Monit. 2017;23:359-365.

    Not in our library10.12659/msm.899719

  244. 244.

    Wang S., Liu J.C., Ju Y., Pellecchia G., Voisin V., Wang D.Y., Leha L.R., Ben-David Y., Bader G.D., Zacksenhaus E. MicroRNA-143/145 loss induces Ras signaling to promote aggressive Pten-deficient basal-like breast cancer. JCI Insight. 2017;2:93313.

    Not in our library10.1172/jci.insight.93313

  245. 245.
    Lessons from miR-143/145: the importance of cell-type localization of miRNAs · 2014
    No notice
  246. 246.

    Xiang Y., Zhang Y., Tang Y., Li Q. MALAT1 Modulates TGF-beta1-Induced Endothelial–to–Mesenchymal Transition through Downregulation of miR-145. Cell Physiol. Biochem. 2017;42:357-372.

    Not in our library10.1159/000477479

  247. 247.

    Ren K., Li Z., Li Y., Zhang W., Han X. Long Noncoding RNA Taurine–Upregulated Gene 1 Promotes Cell Proliferation and Invasion in Gastric Cancer via Negatively Modulating miRNA-145-5p. Oncol. Res. 2017;25:789-798.

    Not in our library10.3727/096504016x14783677992682

  248. 248.

    Hu C.E., Du P.Z., Zhang H.D., Huang G.J. Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145. Cell Physiol. Biochem. 2017;42:13-21.

    Not in our library10.1159/000477107

  249. 249.

    Liu T., Chi H., Chen J., Chen C., Huang Y., Xi H., Xue J., Si Y. Curcumin suppresses proliferation and in vitro invasion of human prostate cancer stem cells by ceRNA effect of miR-145 and lncRNA-ROR. Gene. 2017;631:29-38.

    Not in our library10.1016/j.gene.2017.08.008

  250. 250.

    Xu W., Chang J., Du X., Hou J. Long non-coding RNA PCAT-1 contributes to tumorigenesis by regulating FSCN1 via miR-145-5p in prostate cancer. Biomed. Pharmacother. 2017;95:1112-1118.

    Not in our library10.1016/j.biopha.2017.09.019

  251. 251.

    Kim J., Piao H.-L., Kim B.-J., Yao F., Han Z., Wang Y., Xiao Z., Siverly A.N., Lawhon S.E., Ton B.N., et al. Long noncoding RNA MALAT1 suppresses breast cancer metastasis. Nat. Genet. 2018;50:1705-1715.

    Not in our library10.1038/s41588-018-0252-3

  252. 252.

    Leivonen S.-K., Sahlberg K.K., Mäkelä R., Due E.U., Kallioniemi O., Børresen-Dale A.-L., Perälä M. High–throughput screens identify microRNAs essential for HER2 positive breast cancer cell growth. Mol. Oncol. 2014;8:93-104.

    Not in our library10.1016/j.molonc.2013.10.001

  253. 253.
    MicroRNA-378 limits activation of hepatic stellate cells and liver fibrosis by suppressing Gli3 expression · 2016
    No notice
  254. 254.

    Ikeda K., Horie-Inoue K., Ueno T., Suzuki T., Sato W., Shigekawa T., Osaki A., Saeki T., Berezikov E., Mano H., et al. miR-378a-3p modulates tamoxifen sensitivity in breast cancer MCF-7 cells through targeting GOLT1A. Sci. Rep. 2015;5:13170.

    Not in our library10.1038/srep13170

  255. 255.

    Yadav S., Pandey A., Shukla A., Talwelkar S.S., Kumar A., Pant A.B., Parmar D. miR-497 and miR-302b Regulate Ethanol–induced Neuronal Cell Death through BCL2 Protein and Cyclin D2. J. Biol. Chem. 2011;286:37347-37357.

    Not in our library10.1074/jbc.m111.235531

  256. 256.

    Chen Y., Kuang D., Zhao X., Chen D., Wang X., Yang Q., Wan J., Zhu Y., Wang Y., Zhang S., et al. miR-497-5p inhibits cell proliferation and invasion by targeting KCa3.1 in angiosarcoma. Oncotarget. 2016;7:58148-58161.

    Not in our library10.18632/oncotarget.11252

  257. 257.

    Li D., Zhao Y., Liu C., Chen X., Qi Y., Jiang Y., Zou C., Zhang X., Liu S., Wang X., et al. Analysis of miR-195 and miR-497 Expression, Regulation and Role in Breast Cancer. Clin. Cancer Res. 2011;17:1722-1730.

    Not in our library10.1158/1078-0432.ccr-10-1800

  258. 258.

    Deng S., Li X., Niu Y., Zhu S., Jin Y., Deng S., Chen J., Liu Y., He C., Yin T., et al. miR-652 inhibits acidic microenvironment-induced epithelial-mesenchymal transition of pancreatic cancer cells by targeting ZEB1. Oncotarget. 2015;6:39661-39675.

    Not in our library10.18632/oncotarget.5350

  259. 259.

    Schmalhofer O., Brabletz S., Brabletz T. E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer. Cancer Metast. Rev. 2009;28:151-166.

    Not in our library10.1007/s10555-008-9179-y

  260. 260.

    Mangolini A., Ferracin M., Zanzi M.V., Saccenti E., Ebnaof S.O., Poma V.V., Sanz J.M., Passaro A., Pedriali M., Frassoldati A., et al. Diagnostic and prognostic microRNAs in the serum of breast cancer patients measured by droplet digital PCR. Biomarker Res. 2015;3:12.

    Not in our library10.1186/s40364-015-0037-0

  261. 261.

    Gong C., Tan W., Chen K., You N., Zhu S., Liang G., Xie X., Li Q., Zeng Y., Ouyang N., et al. Prognostic Value of a BCSC-associated MicroRNA Signature in Hormone Receptor-Positive HER2-Negative Breast Cancer. EBioMedicine. 2016;11:199-209.

    Not in our library10.1016/j.ebiom.2016.08.016

  262. 262.

    Singla H., Ludhiadch A., Kaur R.P., Chander H., Kumar V., Munshi A. Recent advances in HER2 positive breast cancer epigenetics: Susceptibility and therapeutic strategies. Eur. J. Med. Chem. 2017;142:316-327.

    Not in our library10.1016/j.ejmech.2017.07.075

  263. 263.

    D’Ippolito E., Iorio M.V. MicroRNAs and triple negative breast cancer. Int. J. Mol. Sci. 2013;14:22202-22220.

    Not in our library10.3390/ijms141122202

  264. 264.

    Sui X., Wang X., Han W., Li D., Xu Y., Lou F., Zhou J., Gu X., Zhu J., Zhang C., et al. MicroRNAs-mediated cell fate in triple negative breast cancers. Cancer Lett. 2015;361:8-12.

    Not in our library10.1016/j.canlet.2015.02.048

  265. 265.

    Lu L., Mao X., Shi P., He B., Xu K., Zhang S., Wang J. MicroRNAs in the prognosis of triple-negative breast cancer: A systematic review and meta-analysis. Medicine (Baltimore). 2017;96:e7085.

    Not in our library10.1097/md.0000000000007085

  266. 266.
    Transcriptional and Post-Transcriptional Gene Regulation by Long Non-Coding RNA · 2017
    No notice
  267. 267.

    Assefa A.T., De Paepe K., Everaert C., Mestdagh P., Thas O., Vandesompele J. Differential gene expression analysis tools exhibit substandard performance for long non-coding RNA-sequencing data. Genome Biol. 2018;19:96.

    Not in our library10.1186/s13059-018-1466-5

  268. 268.

    De Paepe B., Lefever S., Mestdagh P. How long noncoding RNAs enforce their will on mitochondrial activity: Regulation of mitochondrial respiration, reactive oxygen species production, apoptosis, and metabolic reprogramming in cancer. Curr. Genet. 2018;64:163-172.

    Not in our library10.1007/s00294-017-0744-1

  269. 269.

    Gao S., Tian X., Chang H., Sun Y., Wu Z., Cheng Z., Dong P., Zhao Q., Ruan J., Bu W. Two novel lncRNAs discovered in human mitochondrial DNA using PacBio full-length transcriptome data. Mitochondrion. 2018;38:41-47.

    Not in our library10.1016/j.mito.2017.08.002

  270. 270.

    Ørom Ulf A., Shiekhattar R. Long Noncoding RNAs Usher in a New Era in the Biology of Enhancers. Cell. 2013;154:1190-1193.

    Not in our library10.1016/j.cell.2013.08.028

  271. 271.
    The multidimensional mechanisms of long noncoding RNA function · 2017
    No notice
  272. 272.

    Corrà F., Agnoletto C., Minotti L., Baldassari F., Volinia S. The Network of Non-coding RNAs in Cancer Drug Resistance. Front. Oncol. 2018;8:327.

    Not in our library10.3389/fonc.2018.00327

  273. 273.

    Wu Y., Zhang L., Wang Y., Li H., Ren X., Wei F., Yu W., Wang X., Zhang L., Yu J., et al. Long noncoding RNA HOTAIR involvement in cancer. Tumor Biol. 2014;35:9531-9538.

    Not in our library10.1007/s13277-014-2523-7

  274. 274.

    Malih S., Saidijam M., Malih N. A brief review on long noncoding RNAs: A new paradigm in breast cancer pathogenesis, diagnosis and therapy. Tumor Biol. 2016;37:1479-1485.

    Not in our library10.1007/s13277-015-4572-y

  275. 275.

    Zhao Z., Li S., Song E., Liu S. The roles of ncRNAs and histone-modifiers in regulating breast cancer stem cells. Protein Cell. 2016;7:89-99.

    Not in our library10.1007/s13238-015-0199-4

  276. 276.

    Malhotra A., Jain M., Prakash H., Vasquez K.M., Jain A. The regulatory roles of long non-coding RNAs in the development of chemoresistance in breast cancer. Oncotarget. 2017;8:110671-110684.

    Not in our library10.18632/oncotarget.22577

  277. 277.

    Wang J., Ye C., Xiong H., Shen Y., Lu Y., Zhou J., Wang L. Dysregulation of long non-coding RNA in breast cancer: An overview of mechanism and clinical implication. Oncotarget. 2017;8:5508-5522.

    Not in our library10.18632/oncotarget.12537

  278. 278.

    Wang Q., Gao S., Li H., Lv M., Lu C. Long Non-coding RNAs inTriple Negative Breast Cancer. J. Cell Physiol. 2017;232:3226-3233.

    Not in our library10.1002/jcp.25830

  279. 279.

    Warburton A.J., Boone D.N. Insights from Global Analyses of Long Noncoding RNAs in Breast Cancer. Curr. Pathobiol. Rep. 2017;5:23-34.

    Not in our library10.1007/s40139-017-0122-1

  280. 280.

    Koleckova M., Janikova M., Kolar Z. MicroRNAs in triple-negative breast cancer. Neoplasma. 2018;65:1-13.

    Not in our library10.4149/neo_2018_170115n36

  281. 281.

    Richard J.L.C., Eichhorn P.J.A. Deciphering the roles of lncRNAs in breast development and disease. Oncotarget. 2018;9:20179-20212.

    Not in our library10.18632/oncotarget.24591

  282. 282.

    Tian T., Wang M., Lin S., Guo Y., Dai Z., Liu K., Yang P., Dai C., Zhu Y., Zheng Y., et al. The Impact of lncRNA Dysregulation on Clinicopathology and Survival of Breast Cancer: A Systematic Review and Meta-analysis. Mol. Ther. Nucleic Acids. 2018;12:359-369.

    Not in our library10.1016/j.omtn.2018.05.018

  283. 283.

    Bradford J.R., Cox A., Bernard P., Camp N.J. Consensus Analysis of Whole Transcriptome Profiles from Two Breast Cancer Patient Cohorts Reveals Long Non-Coding RNAs Associated with Intrinsic Subtype and the Tumour Microenvironment. PLoS ONE. 2016;11:e0163238.

    Not in our library10.1371/journal.pone.0163238

  284. 284.

    Sun M., Gadad Shrikanth S., Kim D.-S., Kraus W.L. Discovery, Annotation, and Functional Analysis of Long Noncoding RNAs Controlling Cell-Cycle Gene Expression and Proliferation in Breast Cancer Cells. Mol. Cell. 2015;59:698-711.

    Not in our library10.1016/j.molcel.2015.06.023

  285. 285.

    Zhou M., Zhong L., Xu W., Sun Y., Zhang Z., Zhao H., Yang L., Sun J. Discovery of potential prognostic long non-coding RNA biomarkers for predicting the risk of tumor recurrence of breast cancer patients. Sci. Rep. 2016;6:31038.

    Not in our library10.1038/srep31038

  286. 286.

    Guo W., Wang Q., Zhan Y., Chen X., Yu Q., Zhang J., Wang Y., Xu X.-j., Zhu L. Transcriptome sequencing uncovers a three-long noncoding RNA signature in predicting breast cancer survival. Sci. Rep. 2016;6:27931.

    Not in our library10.1038/srep27931

  287. 287.

    Dong Y., Yoshitomi T., Hu J.F., Cui J. Long noncoding RNAs coordinate functions between mitochondria and the nucleus. Epigenetics Chromatin. 2017;10:41.

    Not in our library10.1186/s13072-017-0149-x

  288. 288.

    Rheinbay E., Parasuraman P., Grimsby J., Tiao G., Engreitz J.M., Kim J., Lawrence M.S., Taylor-Weiner A., Rodriguez-Cuevas S., Rosenberg M., et al. Recurrent and functional regulatory mutations in breast cancer. Nature. 2017;547:55-60.

    Not in our library10.1038/nature22992

  289. 289.
    The lncRNA landscape of breast cancer reveals a role for DSCAM-AS1 in breast cancer progression · 2016
    No notice
  290. 290.

    Spector D.L., Lamond A.I. Nuclear Speckles. Cold Spring Harbor Perspect. Biol. 2011;3:A000646.

    Not in our library10.1101/cshperspect.a000646

  291. 291.

    Galganski L., Urbanek M.O., Krzyzosiak W.J. Nuclear speckles: Molecular organization, biological function and role in disease. Nucleic Acids Res. 2017;45:10350-10368.

    Not in our library10.1093/nar/gkx759

  292. 292.

    Li W., Zhang Z., Liu X., Cheng X., Zhang Y., Han X., Zhang Y., Liu S., Yang J., Xu B., et al. The FOXN3-NEAT1-SIN3A repressor complex promotes progression of hormonally responsive breast cancer. J. Clin. Investig. 2017;127:3421-3440.

    Not in our library10.1172/jci94233

  293. 293.

    Zhou S., Wang L., Yang Q., Liu H., Meng Q., Jiang L., Wang S., Jiang W. Systematical analysis of lncRNA-mRNA competing endogenous RNA network in breast cancer subtypes. Breast Cancer Res. Treat. 2018;169:267-275.

    Not in our library10.1007/s10549-018-4678-1

  294. 294.

    Berger A.C., Korkut A., Kanchi R.S., Hegde A.M., Lenoir W., Liu W., Liu Y., Fan H., Shen H., Ravikumar V., et al. A Comprehensive Pan-Cancer Molecular Study of Gynecologic and Breast Cancers. Cancer Cell. 2018;33:690-705.e699.

    Not in our library10.1016/j.ccell.2018.03.014

  295. 295.

    Zhang Y., Wagner E.K., Guo X., May I., Cai Q., Zheng W., He C., Long J. Long intergenic non–coding RNA expression signature in human breast cancer. Sci. Rep. 2016;6:37821.

    Not in our library10.1038/srep37821

  296. 296.

    Xiao B., Zhang W., Chen L., Hang J., Wang L., Zhang R., Liao Y., Chen J., Ma Q., Sun Z., et al. Analysis of the miRNA-mRNA-lncRNA network in human estrogen receptor–positive and estrogen receptor-negative breast cancer based on TCGA data. Gene. 2018;658:28-35.

    Not in our library10.1016/j.gene.2018.03.011

  297. 297.

    Lanz R.B., McKenna N.J., Onate S.A., Albrecht U., Wong J., Tsai S.Y., Tsai M.J., O’Malley B.W. A steroid receptor coactivator, SRA, functions as an RNA and is present in an SRC-1 complex. Cell. 1999;97:17-27.

    Not in our library10.1016/s0092-8674(00)80711-4

  298. 298.

    Murphy L.C., Simon S.L., Parkes A., Leygue E., Dotzlaw H., Snell L., Troup S., Adeyinka A., Watson P.H. Altered expression of estrogen receptor coregulators during human breast tumorigenesis. Cancer Res. 2000;60:6266-6271.

    Not in our library

  299. 299.

    Novikova I.V., Hennelly S.P., Sanbonmatsu K.Y. Structural architecture of the human long non-coding RNA, steroid receptor RNA activator. Nucleic Acids Res. 2012;40:5034-5051.

    Not in our library10.1093/nar/gks071

  300. 300.

    Leygue E. Steroid receptor RNA activator (SRA1): Unusual bifaceted gene products with suspected relevance to breast cancer. Nucl. Recept. Signal. 2007;5:e006.

    Not in our library10.1621/nrs.05006

  301. 301.
    New Insights Into the Long Non-coding RNA SRA: Physiological Functions and Mechanisms of Action · 2018
    Not checked
  302. 302.

    Zhang X., Hamblin M.H., Yin K.J. The long noncoding RNA Malat1: Its physiological and pathophysiological functions. RNA Biol. 2017;14:1705-1714.

    Not in our library10.1080/15476286.2017.1358347

  303. 303.

    Huang S.K., Luo Q., Peng H., Li J., Zhao M., Wang J., Gu Y.Y., Li Y., Yuan P., Zhao G.H. A Panel of Serum Noncoding RNAs for the Diagnosis and Monitoring of Response to Therapy in Patients with Breast Cancer. Med. Sci. Monit. 2018;24:2476-2488.

    Not in our library10.12659/msm.909453

  304. 304.
    Z Probe, An Efficient Tool for Characterizing Long Non-Coding RNA in FFPE Tissues · 2018
    Not checked
  305. 305.

    Ong M.S., Cai W., Yuan Y., Leong H.C., Tan T.Z., Mohammad A., You M.L., Arfuso F., Goh B.C., Warrier S., et al. ‘Lnc’-ing Wnt in female reproductive cancers: Therapeutic potential of long non-coding RNAs in Wnt signalling. Br. J. Pharmacol. 2017;174:4684-4700.

    Not in our library10.1111/bph.13958

  306. 306.

    Arun G., Diermeier S., Akerman M., Chang K.C., Wilkinson J.E., Hearn S., Kim Y., MacLeod A.R., Krainer A.R., Norton L., et al. Differentiation of mammary tumors and reduction in metastasis upon Malat1 lncRNA loss. Genes Dev. 2016;30:34-51.

    Not in our library10.1101/gad.270959.115

  307. 307.

    Nik–Zainal S., Davies H., Staaf J., Ramakrishna M., Glodzik D., Zou X., Martincorena I., Alexandrov L.B., Martin S., Wedge D.C., et al. Landscape of somatic mutations in 560 breast cancer whole-genome sequences. Nature. 2016;534:47-54.

    Not in our library10.1038/nature17676

  308. 308.

    Chen R., Liu Y., Zhuang H., Yang B., Hei K., Xiao M., Hou C., Gao H., Zhang X., Jia C., et al. Quantitative proteomics reveals that long non-coding RNA MALAT1 interacts with DBC1 to regulate p53 acetylation. Nucleic Acids Res. 2017;45:9947-9959.

    Not in our library10.1093/nar/gkx600

  309. 309.
    Functional and prognostic significance of long non-coding RNA MALAT1 as a metastasis driver in ER negative lymph node negative breast cancer · 2016
    No notice
  310. 310.
    CCAT2 , a novel long non-coding RNA in breast cancer: expression study and clinical correlations · 2013
    No notice
  311. 311.

    Cai Y., He J., Zhang D. Long noncoding RNA CCAT2 promotes breast tumor growth by regulating the Wnt signaling pathway. OncoTargets Ther. 2015;8:2657-2664.

    Not in our library10.2147/ott.s90485

  312. 312.

    Wu Z.J., Li Y., Wu Y.Z., Wang Y., Nian W.Q., Wang L.L., Li L.C., Luo H.L., Wang D.L. Long non–coding RNA CCAT2 promotes the breast cancer growth and metastasis by regulating TGF-beta signaling pathway. Eur. Rev. Med. Pharmacol. Sci. 2017;21:706-714.

    Not in our library

  313. 313.

    Deng X., Zhao Y., Wu X., Song G. Upregulation of CCAT2 promotes cell proliferation by repressing the P15 in breast cancer. Biomed. Pharmacother. 2017;91:1160-1166.

    Not in our library10.1016/j.biopha.2017.05.030

  314. 314.

    Sandhu C., Garbe J., Bhattacharya N., Daksis J., Pan C.H., Yaswen P., Koh J., Slingerland J.M., Stampfer M.R. Transforming growth factor beta stabilizes p15INK4B protein, increases p15INK4B-cdk4 complexes, and inhibits cyclin D1-cdk4 association in human mammary epithelial cells. Mol. Cell Biol. 1997;17:2458.

    Not in our library10.1128/mcb.17.5.2458

  315. 315.

    Huan J., Xing L., Lin Q., Xui H., Qin X. Long noncoding RNA CRNDE activates Wnt/beta–catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer. Am. J. Trans. Res. 2017;9:1977-1989.

    Not in our library

  316. 316.

    Nusse R., Clevers H. Wnt/β-Catenin Signaling, Disease, and Emerging Therapeutic Modalities. Cell. 2017;169:985-999.

    Not in our library10.1016/j.cell.2017.05.016

  317. 317.

    Holland J.D., Klaus A., Garratt A.N., Birchmeier W. Wnt signaling in stem and cancer stem cells. Curr. Opin. Cell Biol. 2013;25:254-264.

    Not in our library10.1016/j.ceb.2013.01.004

  318. 318.

    Wang Y., Xu Z., Jiang J., Xu C., Kang J., Xiao L., Wu M., Xiong J., Guo X., Liu H. Endogenous miRNA Sponge lincRNA-RoR Regulates Oct4, Nanog, and Sox2 in Human Embryonic Stem Cell Self–Renewal. Dev. Cell. 2013;25:69-80.

    Not in our library10.1016/j.devcel.2013.03.002

  319. 319.

    Hou P., Zhao Y., Li Z., Yao R., Ma M., Gao Y., Zhao L., Zhang Y., Huang B., Lu J. LincRNA–ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis. Cell Death Dis. 2014;5:e1287.

    Not in our library10.1038/cddis.2014.249

  320. 320.

    Hou L., Tu J., Cheng F., Yang H., Yu F., Wang M., Liu J., Fan J., Zhou G. Long noncoding RNA ROR promotes breast cancer by regulating the TGF-β pathway. Cancer Cell Int. 2018;18:142.

    Not in our library10.1186/s12935-018-0638-4

  321. 321.

    Zhang J.J., Guo S.H., Jia B.Q. Down-regulation of long non–coding RNA MEG3 serves as an unfavorable risk factor for survival of patients with breast cancer. Eur. Rev. Med. Pharmacol. Sci. 2016;20:5143-5147.

    Not in our library

  322. 322.

    Zhang W., Shi S., Jiang J., Li X., Lu H., Ren F. LncRNA MEG3 inhibits cell epithelial-mesenchymal transition by sponging miR-421 targeting E-cadherin in breast cancer. Biomed. Pharmacother. 2017;91:312-319.

    Not in our library10.1016/j.biopha.2017.04.085

  323. 323.
    Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway · 2017
    Not checked
  324. 324.

    Malissovas N., Ninou E., Michail A., Politis P.K. Targeting Long Non-Coding RNAs in Nervous System Cancers: New Insights in Prognosis, Diagnosis and Therapy. Curr. Med. Chem. 2018.

    Not in our library10.2174/0929867325666180831170227

  325. 325.

    Deng Y., Luo S., Zhang X., Zou C., Yuan H., Liao G., Xu L., Deng C., Lan Y., Zhao T., et al. A pan–cancer atlas of cancer hallmark–associated candidate driver lncRNAs. Mol. Oncol. 2018;12:1980-2005.

    Not in our library10.1002/1878-0261.12381

  326. 326.

    Colombo M., Raposo G., Thery C. Biogenesis, secretion, and intercellular interactions of exosomes and other extracellular vesicles. Annu. Rev. Cell Dev. Biol. 2014;30:255-289.

    Not in our library10.1146/annurev-cellbio-101512-122326

  327. 327.

    Melo Sonia A., Sugimoto H., O’Connell Joyce T., Kato N., Villanueva A., Vidal A., Qiu L., Vitkin E., Perelman Lev T., Melo Carlos A., et al. Cancer Exosomes Perform Cell-Independent MicroRNA Biogenesis and Promote Tumorigenesis. Cancer Cell. 2014;26:707-721.

    Not in our library10.1016/j.ccell.2014.09.005

  328. 328.
    Extracellular vesicles as circulating cancer biomarkers: opportunities and challenges · 2018
    No notice
  329. 329.

    Li S., Li Y., Chen B., Zhao J., Yu S., Tang Y., Zheng Q., Li Y., Wang P., He X., et al. exoRBase: A database of circRNA, lncRNA and mRNA in human blood exosomes. Nucleic Acids Res. 2018;46:D106-D112.

    Not in our library10.1093/nar/gkx891

  330. 330.

    O’Brien K., Rani S., Corcoran C., Wallace R., Hughes L., Friel A.M., McDonnell S., Crown J., Radomski M.W., O’Driscoll L. Exosomes from triple-negative breast cancer cells can transfer phenotypic traits representing their cells of origin to secondary cells. Eur. J. Cancer. 2013;49:1845-1859.

    Not in our library10.1016/j.ejca.2013.01.017

  331. 331.

    Sansone P., Savini C., Kurelac I., Chang Q., Amato L.B., Strillacci A., Stepanova A., Iommarini L., Mastroleo C., Daly L., et al. Packaging and transfer of mitochondrial DNA via exosomes regulate escape from dormancy in hormonal therapy–resistant breast cancer. Proc. Natl. Acad. Sci. USA. 2017;114:E9066-E9075.

    Not in our library10.1073/pnas.1704862114

  332. 332.

    Halvaei S., Daryani S., Eslami-S Z., Samadi T., Jafarbeik-Iravani N., Bakhshayesh T.O., Majidzadeh-A K., Esmaeili R. Exosomes in Cancer Liquid Biopsy: A Focus on Breast Cancer. Mol. Ther. Nucleic Acids. 2018;10:131-141.

    Not in our library10.1016/j.omtn.2017.11.014

  333. 333.
    Plasma exosome microRNAs are indicative of breast cancer · 2016
    No notice
  334. 334.

    Sempere L.F., Keto J., Fabbri M. Exosomal MicroRNAs in Breast Cancer towards Diagnostic and Therapeutic Applications. Cancers. 2017;9:71.

    Not in our library10.3390/cancers9070071

  335. 335.

    Wei Y., Lai X., Yu S., Chen S., Ma Y., Zhang Y., Li H., Zhu X., Yao L., Zhang J. Exosomal miR-221/222 enhances tamoxifen resistance in recipient ER-positive breast cancer cells. Breast Cancer Res. Treat. 2014;147:423-431.

    Not in our library10.1007/s10549-014-3037-0

  336. 336.

    Xu C.G., Yang M.F., Ren Y.Q., Wu C.H., Wang L.Q. Exosomes mediated transfer of lncRNA UCA1 results in increased tamoxifen resistance in breast cancer cells. Eur. Rev. Med. Pharmacol. Sci. 2016;20:4362-4368.

    Not in our library

  337. 337.

    Muluhngwi P., Alizadeh-Rad N., Vittitow S.L., Kalbfleisch T.S., Klinge C.M. The miR-29 transcriptome in endocrine-sensitive and resistant breast cancer cells. Sci. Rep. 2017;7:5205.

    Not in our library10.1038/s41598-017-05727-w

  338. 338.

    Wu C., Luo J. Long Non–Coding RNA (lncRNA) Urothelial Carcinoma-Associated 1 (UCA1) Enhances Tamoxifen Resistance in Breast Cancer Cells via Inhibiting mTOR Signaling Pathway. Med. Sci. Monit. 2016;22:3860-3867.

    Not in our library10.12659/msm.900689

  339. 339.

    Zhang P., Zhou H., Lu K., Lu Y., Wang Y., Feng T. Exosome-mediated delivery of MALAT1 induces cell proliferation in breast cancer. OncoTargets Ther. 2018;11:291-299.

    Not in our library10.2147/ott.s155134

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