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Micro RNA ‐145: a potent tumour suppressor that regulates multiple cellular pathways

Shi‐Yun Cui, Rui Wang, Long‐Bang Chen

Journal of Cellular and Molecular Medicine · 2014 · Review · CC BY

Abstract

Micro RNA s are endogenous, small (18–25 nucleotides) non‐coding RNA s, which regulate genes expression by directly binding to the 3′‐untranslated regions of the target messenger RNA s. Emerging evidence shows that alteration of micro RNA s is involved in cancer development. Micro RNA ‐145 is commonly down‐regulated in many types of cancer, regulating various cellular processes, such as the cell cycle, proliferation, apoptosis and invasion, by targeting multiple oncogenes. This review aims to summarize the recent published literature on the role of micro RNA ‐145 in regulating tumourigenesis and progression, and explore its potential for cancer diagnosis, prognosis and treatment.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 24, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

1For a long time, protein-coding genes have been considered the principal effectors and regulators of tumourigenesis. However, this concept has been revised recently. Non-coding RNAs have emerged as active modulators of the protein-coding gene function. Identification of non-coding RNA-based epigenetic regulatory networks has opened up an entirely new area of cancer research.

2Among these, microRNAs (miRNAs) are the most-studied non-coding RNAs. They are short, 18–25 nucleotide, non-coding RNAs, which bind to target messenger RNAs (mRNAs), usually in their 3′-untranslated regions (UTR), and inhibit their expression by either inducing their degradation or repressing their translation. Since their discovery in 1993,, over 2500 miRNAs have been identified in the human genome, which are thought to regulate more than 30% of the protein-coding genes. Thus, they have emerged as integral components of nearly every biological process, including cell proliferation, migration, differentiation, apoptosis and angiogenesis. Recent evidence has shown that altered expressions of miRNAs are associated with carcinogenesis and development of various cancers. By regulating hundreds to thousands of potential target genes, miRNAs form a novel layer of the complicated regulatory network in cells. Thus, disorder of miRNA expression can lead to pathological changes in cells, ultimately contributing to the development of cancers.

3MiR-145 was first predicted based on its homology to a verified miRNA from mouse, and was subsequently verified in humans, with significantly reduced levels in colorectal cancer. Slightly over half (52.5%) of miRNA genes are located in cancer-associated regions or fragile sites in the genome. Consistently, miR-145 is located on chromosome 5 (5q32-33), a well-known fragile site in the human genome, and is suggested to be co-transcribed with miR-143. Down-regulation of miR-145 has been observed in many types of cancers, suggesting that it may serve as a tumour suppressor. So far, miR-145 has been shown to be involved in regulating various cellular processes, such as the cell cycle, proliferation, apoptosis and invasion, by targeting multiple oncogenes. Moreover, reduced expression of miR-145 is associated with a worse prognosis for many cancers, indicating that it may serve as a potential cancer biomarker and an attractive target for cancer therapy. This review aims to summarize recent research on the physiology and pathological functions of miR-145 and its implications for clinical therapy.

MiR-145 Biogenesis

4A unique biogenesis pathway produces miRNAs. RNA pol II transcribes most miRNAs from introns of protein-coding genes as long primary transcripts (pri-miRNAs) with a 5′ m7G cap and a 3′ poly-A tail. After transcription, pri-miRNAs undergo at least three steps before becoming the mature single-stranded form.

5The pri-miRNA is cleaved into a stem-loop structure containing 60–70-nt (precursor) pre-miRNAs by the nuclear microprocessor complex, which comprises the RNase III enzyme Drosha (RNASEN), the DGCR8 (DiGeorge critical region 8), a double-stranded RNA binding protein and multiple RNA-associated proteins such as the DEAD-box RNA helicases p68 and p72. P68 and p72 are required for the maturation of miR-145, but not for all miRNAs. They enhance pre-miRNA processing by unwinding double-stranded stem loop-containing pre-miRNAs. After nuclear processing, the pre-miRNA is exported into the cytoplasm by RAN-GTPase/Exportin5 (Expo5) for further processing. Another RNase type III protein, Dicer, together with its partner TAR (HIV) RNA binding protein (TRBP), removes the loop region from the pre-miRNA and cleaves it into a ∼22-nt double-stranded RNA product containing two forms of mature miRNAs that can be cleaved from either the 5′ or 3′ arm extending out from the stem loop of the pre-miRNA –. For example, mature miR-145 has two different forms, 5p and 3p, according to which side of the strand they were derived from (Fig.1).

6The guide strand or mature miRNA is bound by Argonaute (Ago) to form a miRNA-induced silencing complex (miRISC), which targets the 3′-UTR of the complementary mRNAs for regulation, whereas the passenger strand is usually degraded. The specificity of miRNA targeting is defined by how complementary are the ‘seed’ sequence (positions 2 to 8 from the 5′end of the miRNA) and the ‘seed-match’ sequence (generally in the 3′ UTR of the target mRNA). A perfect match between miRNAs and mRNA sequences promotes the degradation of mRNAs by Ago1/2, while an imperfect match usually leads to translational repression. The imperfect nature of the miRNA:mRNA interaction means that a single miRNA can potentially target tens to hundreds of mRNAs.

Down-regulation of miR-145 in cancer

7Reduced expression of miR-145 has been reported in many types of cancer. The first report, from Michael et al., observed low expression of miR-145 in colonic adenocarcinoma compared with mucosa. This result was confirmed by further research in different cancer cell lines, including both solid and blood malignancies (Table1). This evidence indicated widespread deregulation of miR-145 levels in various cancers.

8However, the mechanisms responsible for its down-regulation are largely unknown. Gene expression regulation is a multilayered network, where transcription is a major regulatory step for the biosynthesis of miRNAs. A couple of transcriptional factors have been identified that modulate the expression of miR-145, and an epigenetic mechanism also plays an important role in the silencing of miR-145. After transcription, pri-miR-145 undergoes several processing steps before its maturation, where some factors also play essential roles at the post-transcriptional level (Fig.2).

9p53 is a master tumour suppressor that controls diverse cellular pathways. Recent evidence indicated that some miRNAs are also regulated by p53, such as miR-34, miR-192/215, miR-107 and miR-145,. Sachdeva et al. found that p53 could increase miR-145 expression by directly binding to the p53 response elements-2 (p53RE-2) in the miR-145 promoter, which was possibly the mechanism of p53-mediated repression of c-Myc. Low miR-145 expression was demonstrated in both laser capture microdissected prostate tissues and 47 cancer cell lines, coupled with p53 mutations. Glucocorticoid-induced human papillomavirus oncoprotein E6 (HPV-E6) activation suppressed p53 and miR-145 expression in cervical cancer. The tumour-suppressive effect of miR-145 is dependent on p53 activation in some tumours,. Furthermore, Suzuki et al. discovered that p53 could facilitate Drosha-mediated pri-miR-145 processing through an association with the DEAD-box RNA helicase p68 (also known as DDX5), a key component of the Drosha complex, indicating post-transcriptional regulation also plays an important role in the modulation of miR-145 expression by p53. Interestingly, there seems to be positive feedback regulation between miR-145 and p53, partially by impairing the murine double minute 2 (MDM2)-p53 feedback loop,. This could partially explain why miR-145 is frequently down-regulated in p53-mutated cancers.

10The Kras gene mutation is commonly found in many malignancies, and can stimulate a number of downstream effectors, including the mitogen-activated protein kinase (MAPK) and phosphoinositide-3-kinase (PI3K) pathways, ultimately promoting cellular proliferation, survival and motility. Kent et al. showed that Kras signalling led to repression of the miR-143/145 cluster by activating Ras-responsive element-binding protein 1 (RREB1) in pancreatic cancers. In turn, miR-143 and miR-145 targeted KRAS and RREB1, establishing a feedback circuit of Ras signalling. The same results were also obtained in colorectal cancers. Consistent with this, there is an inverse correlation between KRAS and the miR-143/145 cluster in colorectal cancer.

11However, the reason for the low expression of miR-145 in tumours with wild-type p53 is unclear, implying that factor(s) other than p53 are involved in miR-145 regulation. In addition to p53, other transcription factors participate in the regulation of miR-145, including CCAAT/enhancer-binding protein-beta (C/EBP-β), beta-catenin/T cell factor 4 (TCF4) and forkhead transcription factors of the O class 1 and 3 (FoxO1 and FoxO3) –. In addition, DNA methylation in the upstream sequence of miR-145 contributes to the down-regulation of miR-145 in prostate cancer, and, importantly, interferes with the binding of p53 to the p53 response element in the upstream region of miR-145.

12Post-transcriptional regulation is also critical for miR-145 expression. Apart from p53, Breast cancer 1 (BRCA1) recognizes the root of the stem-loop structure of pri-miR-145, directly associates with Drosha and DDX5 of the Drosha complex, and interacts with Smad3, p53, and DHX9 RNA helicase, promoting miR-145 processing. Similarly, the p38 MAPK-MK2 signalling pathway promotes miR-145 biogenesis by facilitating the nuclear localization of DDX5. Conversely, BCDIN3D is a methyltransferase that modifies the 5′-monophosphate end of miRNAs, including pre-miR-145, which affects their recognition by Dicer. BCDIN3D depletion reduced the level of pre-miR-145 and increased the level of mature miR-145 in breast cancer cells. DEAD-box RNA helicase 6 (DDX6) preferentially increases the instability of the host gene product of miR-145 (NCR143/145) by promoting the assembly of processing bodies (P-bodies), thus negatively regulating miR-145 expression at the post-transcriptional level. Doublecortin-like kinase 1 (DCLK1) post-transcriptionally regulates miR-145 in pancreatic cancer; however, the mechanism is unclear.

The functions and pathways involving miR-145 targets

13To date, numerous oncogenic genes have been confirmed as targets for miR-145, which cover multiple biological pathways, including proliferation, invasion, differentiation, angiogenesis and cancer-related viruses, supporting the proposed tumour-suppressor role of miR-145 in cancers (Table2). For example, miR-145 could suppress cancer cell proliferation by targeting growth factor-related genes such as IRS-1, IGF-IR or epidermal growth factor receptor (EGFR) –. Moreover, inducing cell apoptosis and cell cycle arrest by inhibiting DFF45, CBFB, CLINT1, PPP3CA or c-Myc also contributes to miR-145-mediated tumour growth suppression,,. Direct regulation of some oncogenes involved in cancer cell invasion and metastasis, like MUC1, FSCN1, NEDD9 and SOX9, by miR-145 has been identified in many cancers –. In addition, there is evidence that miR-145 has an important role in regulating cell differentiation by targeting core reprogramming factors, including OCT4, SOX2 and KLF4,. Meanwhile, miR-145 could retard angiogenesis process by targeting VEGF, hypoxia-inducible factor 1α (HIF-1α) or N-RAS –. What is more, some cancer-related virus genes, such as infected-cell polypeptide 4 (ICP4), have been validated as targets for miR-145. By regulating these target genes, miR-145 exerts a potent tumour-suppressive effect. However, the number of target genes is still growing, indicating a complicated regulatory network for miR-145.

MiR-145 in tumour growth inhibition

14The tumour-suppressive function of miR-145 is related to its regulation of cell proliferation. The first report describing tumour growth inhibition by miR-145 was from a study in colon cancer cells, where miR-145 suppressed tumour growth by targeting insulin receptor substrate-1 (IRS-1). MiR-145-mediated tumour growth inhibition was also found in cervical cancer and lung adenocarcinomas,. IRS1 is also involved in miR-145′s ability to suppress cell proliferation, anchorage-independent growth and cell motility in gastric cancer and hepatocellular carcinoma. Interestingly, the insulin-like growth factor I receptor (IGF-IR) is also a predominant target of miR-145, by which miR-145 suppresses the tumour growth of colorectal cancer and hepatocellular carcinoma, suggesting that the IGR/IRS1 pathway plays an important role in miR-145-mediated anti-proliferative function,.

15Furthermore, Cho et al. described strong suppression of tumour growth by miR-145 in lung adenocarcinoma patients with an EGFR mutation. They further stated that EGFR and nucleoside diphosphate-linked moiety X-type motif 1 (NUDT1) were regulated by miR-145. Similarly, forced expression of miR-145 could suppress EGF-induced growth in vitro and tumour xenograft growth in vivo, suggesting that the EGFR pathway might be involved in the tumour-suppressive effect of miR-145. In addition, EGFR-independent activity of the PI3K/Akt or Ras/ERK pathway contributes to EGFR-targeted agents-resistance in non-small cell lung cancer (NSCLC) cell lines. MiR-145 could enhance the cytotoxicity of gefitinib by reducing the activation of Akt rather than ERK. Further research indicated that miR-145 indirectly regulates the Akt pathway by directly targeting Integrin-Linked Kinase (ILK), and co-treatment with miR-143 and miR-145 synergistically inhibited cell growth in bladder cancer cells.

16MiR-145 induces caspase-3-dependent apoptosis in colon cancer by targeting DNA fragmentation factor 45 (DFF45), which is the substrate of caspase-3 and whose cleavage by caspase-3 during apoptosis releases DFF40, which degrades chromosomal DNA into nucleosomal fragments. Ostenfeld et al. reported that miR-145 induced caspase-dependent and-independent cell death in human urothelial cancer cells by targeting Clathrin Interactor 1 (CLINT1), core-binding factor β subunit (CBFB) and protein phosphatase 3 catalytic subunit α isoform (PPP3CA). However, two other reports also suggested a role of miR-145 in Tumour Necrosis Factor-related Apoptosis-Inducing Ligand (TRAIL)-induced apoptotic cell death,. In bladder cancer, miR-145 induces interferon (IFN)-beta-mediated apoptosis by targeting the suppressor of cytokine signalling 7 (socs7). Moreover, over-expression of miR-145 increased the cleaved-PARP expression and induced apoptosis in breast cancer cells, by repression of oestrogen receptor-α (ER-α) and up-regulation of the TP53 transcriptional targets, such as p53 up-regulated modulator of apoptosis (PUMA) and P21, indicating that miR-145 activates the TP53 pathway and suppresses ER-α.

17Sachdeva et al. revealed that miR-145 causes cell cycle arrest at G0-G1 phase and a decrease in S-phase, partially through silencing the expression of c-Myc. Consistent with these results, the miR-145-induced G1/S-phase arrest is mediated by c-Myc in NSCLC, with downstream regulation of CDK4. C-Myc, along with the DNA-binding protein Miz-1, binds to the p21(Cip1) promoter and blocks its transcription induction by p53 and other activators, thus preventing p53-mediated apoptosis. Therefore, forced expression of miR-145 could restore p53-induced cell cycle arrest, which was likely to be caused, in part, by silencing c-Myc. Moreover, the regulation of c-Myc by miR-145 has been associated with proliferation, apoptosis and metastasis in various cancers, including colon cancer, NSCLC, ovarian cancer, breast cancer, oesophageal and oral squamous cell carcinoma,,–, highlighting the potent tumour-suppressive effect of the miR-145/c-Myc pathway.

18MiR-145 regulates certain oncogenic transcription factors to suppress cell growth. For example, E-26 (ETS) transcriptional factors are well-known proto-oncogenes with mitogenic and transforming activity. Some members of the ETS family, such as the Friend leukaemia virus integration 1 (FLI1) and the v-ets avian erythroblastosis virus E26 oncogene homologue (ERG), were identified as targets of miR-145, and are involved in miR-145-mediated apoptosis and repression of cell proliferation in colon and prostate cancer, respectively,. Moreover, miR-145 regulates the expression of Ets1 and its downstream genes, matrix metalloproteinase-1 (MMP-1) and-9, thus inhibiting the invasion, metastasis and angiogenesis of gastric cancer cells. Interestingly, EWS-FLI1 is a chromosome translocation-derived chimeric transcription factor that is the major driver of the proliferation of Ewing's sarcoma. The EWS-FLI1 gene shares the same 3′-UTR with the FLI1 gene; therefore, its relationship with miR-145 has been explored in Ewing's sarcoma. It transpired that there is feedback regulation between EWS-FLI1 and miR-145 in Ewing's sarcoma growth regulation. MicroRNA/mRNA profiling in ovarian cancer suggested a negative correlation between miR-145 and a transcriptional factor, E2F3, but it is not clear whether there is a direct regulation.

19In addition, there are multiple oncogenic genes that have been identified as targets of miR-145, including RTKN, YES, STAT1, HDAC2 and PAI-1 –, contributing to its tumour growth-suppressive effect.

MiR-145 in cancer invasion and metastasis

20MiR-145 was observed to be differentially expressed in node-negative patients or node-positive gastric cancer patients. Similarly, effusion samples contain lower miR-145 levels than primary ovarian cancers, suggesting a role of miR-145 in cancer progression. MiR-145 is also a biomarker in the transition from localized prostate adenocarcinoma to metastasis. Restoration of miR-145 expression could inhibit the migration and invasion ability of cancer cells,. These reports provide a new insight into miR-145-mediated suppression of invasion and metastasis. Mucin 1 (MUC1) is co-expressed with β-catenin at the invasion front of colorectal carcinoma, and is associated with progression of disease and poor prognosis. In addition, MUC1 interacts with β-catenin, promoting invasion of breast cancer. Therefore, it is considered as an important metastasis gene. MiR-145 suppresses cell invasion and lung metastasis of breast cancer in vitro and in vivo, and this effect is, in part, attributed to silencing of MUC1,,. Recent research also described the relationship between miR-145 and some adhesion or cytoskeleton molecules. For example, Fascin homologue 1 (FSCN1), an actin-binding protein, is a candidate target gene of miR-145. MiR-145 participates in the modulation of proliferation and invasion by targeting FSCN1 in various cancers, including bladder cancer, oesophageal squamous cell carcinoma, prostate cancer, melanoma cells and breast cancer cells,–. Notably, a more cortical actin distribution, reduced actin stress fibres and filopodia formation, and nuclear rotation were observed in miR-145-transfected breast cancer cells by immunofluorescence microscopy. Their effects were partially attributed to the miR-145-dependent regulation of Junctional Adhesion Molecule A (JAM-A) and FSCN1, which contribute to the cytoskeletal rearrangements and cell motility. Similar to FSCN1, another actin-binding protein, the SWAP switching B-cell complex 70 kD subunit (SWAP70), was confirmed as a target of miR-145, which is associated with miR-145's modulation of cell migration and invasion in prostate cancer. Human enhancer of filamentation 1(HEF1/CAS-L/NEDD9) is a non-catalytic scaffolding protein that interacts with FAK and Src to create binding sites for effector proteins, such as Rac and the Cas-Crk complex. It has been proposed to be involved in cancer invasion and epithelial-mesenchymal transition (EMT),. Recent research demonstrated that NEDD9 promotes the invasiveness of glioblastoma under the regulation of miR-145, and low expression of miR-145 in glioblastoma was associated with a more aggressive phenotype. NEDD9 also mediated the function of miR-145 in regulating EMT, migration and invasion in prostate cancer and renal cell carcinoma,. MiR-145 also targets N-cadherin, a calcium-dependent cell adhesion molecule associated with an increased invasive potential, suppressing invasion and metastasis, rather than inhibiting cell proliferation in gastric cancer. Besides direct regulation, the impact of miR-145 on E-cadherin and N-cadherin expression in glioma is partially caused by its regulation of Adducin 3 (ADD3), a cell adhesion-associated molecule. Another target gene, Metalloproteinase 17 (ADAM17), is an important member of the ADAM family involved in cancer invasion that plays an important role in the effects of miR-145 on proliferation and migration in renal cancer and glioma cells,. SRY (sex determining region Y) box 9 (SOX9), a positive transcription factor of ADAM17, is also a target of miR-145 and participates in the regulation of tumour-initiating cell and IL-6-mediated paracrine effects in head and neck cancer. In addition, miR-145 regulates glioma cell migration by targeting connective tissue growth factor (CTGF), a member of the CCN family, which decreases the expression and phosphorylation of FAK and the expression of secreted protein acidic and rich in cysteine, two important cell migration-relative pathways. Moreover, miR-145 directly targets catenin δ-1 and impairs nuclear translocation of β-catenin by disturbing the nuclear import of p21-activated kinase 4 (PAK4), leading to the down-regulation of downstream target genes c-Myc and CyclinD1, which contribute to the attenuation of cell migration and invasion activities in colon cancer. PAK4 was also proposed as a direct target of miR-145. The above evidence strongly supports the anti-metastatic role of miR-145 in cancer cells.

21By contrast, several reports describe the oncogenic effect of miR-145. Although miR-145 and miR-143 are both down-regulated in colorectal cancer samples compared with normal tissues, miR-145 promoted proliferation and morphology in a metastatic colorectal cancer cell line while miR-143 did the contrary. Bioinformatic analysis found that miR-145 targets are differentially expressed between metastatic and non-metastatic isogenic cell line models. MiR-145, along with miR-143, was over-expressed in a serial selected invasive glioblastoma cell line, and knocking down both of them demonstrated a synergistic anti-invasive effect. Therefore, the role of miR-145 in metastasis may be tissue-specific, and targeting miR-145 in metastatic cancers requires discreet consideration.

MiR-145 in the differentiation of cancer stem cells

22Cancer stem cells (CSCs) are a minority population of cells within a tumour, and are characterized by self-renewal and high tumourigenic capacity. Recent evidence suggests that CSCs might be formed during the process of EMT, and play important roles in development, recurrence, metastasis and drug resistance of cancer,. Embryonic pluripotent stem cells share a similar capacity for self-renewal and transformation into differentiated cells with CSCs, which are maintained by a group of transcription factors in both mice and human, including OCT4, SOX2 and Kruppel-like factor 4 (KLF4) –. Xu et al. revealed a direct link between miR-145 and these core reprogramming factors. Further research confirmed the reciprocal negative regulation of miR-145 and OCT4 and SOX2,. Given the role of miR-145 in silencing pluripotency during embryonic stem cell differentiation, it is not surprising that miR-145 also inhibits the proliferation of CSCs and induces differentiation, contributing to suppression of tumour growth, migration and EMT,,–. Moreover, forced expression of miR-145 suppressed tumour sphere formation and expression of CSC markers and ‘stemness’ factors, including CD133, CD44, Oct4, c-Myc and Klf4 in prostate cancer cells, and inhibited bone invasion and tumourigenesis of prostate cancer in vivo.

MiR-145 in angiogenesis

23Angiogenesis is a process by which new blood vessels sprout from existing vasculature. It is vital for tumour growth and metastasis, because cancer cells cannot grow beyond 2 mm3 without vascular support. MiR-145 exhibits tumour-suppressive functions by modulating angiogenesis. VEGF, one of the strongest angiogenic factors, is a direct target of miR-145, regulating the invasion and metastasis of osteosarcoma cells, which implies a role of miR-145 in modulating tumour angiogenesis. In addition, miR-145 decreases HIF-1α expression, a major transcriptional regulator of VEGF in response to hypoxia, as well as decreasing VEGF expression by targeting p70S6K1 in colorectal cancer, leading to the inhibition of tumour growth and angiogenesis. In addition to VEGF, N-RAS was identified as a target of miR-145, which plays a pivotal role in its anti-angiogenic effect in breast cancer. Further research showed that miR-145 inhibits N-RAS and IRS1 expression to suppress AKT and ERK1/2 activation and VEGF expression in colorectal cancer.

MiR-145 and cancer-associated virus

24Surprisingly, miR-145 plays an important role in interfering with the cancer-associated viruses-mediated tumourigenesis process. In head and neck squamous cell carcinoma (HNSCC), the HPV-positive (HPV+) samples had a different miRNA profile from the HPV-negative (HPV−) samples, which was more similar to the miRNA profile of cervical squamous cell carcinoma than HPV-HNSCC. Among the HPV core miRNAs was the miR-143/145 cluster, suggesting miR-145 as a potential HPV-specific tumour marker. In addition, miR-145 could target a herpes simplex virus-1 essential viral gene, ICP4, to create CMV-ICP4-143T and CMV-ICP4-145T amplicon viruses, leading to restriction of viral replication and oncolysis of prostate cancer cells while sparing normal tissues, both in vitro and in vivo.

MiR-145 in cancer diagnosis and prognosis

25Specific miRNAs have been found to be differentially expressed in the majority of tumour cases; therefore, miRNA expression patterns are capable of distinguishing between malignant and non-malignant tissue. MiR-145 is differentially expressed in breast cancers and normal breast tissues, and its down-regulation is closely associated with invasive breast cancer pathobiological features. A noticeable decrease in miR-145 expression was observed in hyperplastic, probable pre-neoplastic, ducts present in normal breast tissues compared with normal ducts, as well as in carcinoma in situ and invasive carcinoma, compared with normal tissues. In another study, miR-145 was identified as one of the eight basal cell type-specific miRNAs in breast cancer. In addition, Wach et al. demonstrated that miR-145 was the best discriminating miRNA that could correctly classify 71% of prostate cancer tissue samples and, when combined with miR-375 and miR-143, the correct classification rate of miR-145 reached almost 78%, suggesting that miR-145 could serve as valuable biomarker for the diagnosis of prostate cancer. Another independent study obtained an area under the curve (AUC) of 0.74 for the ability of miR-145 expression to discriminate between prostate cancer and non-tumour tissues. MiR-145 can also distinguish between subtypes of certain tumours, such as intestinal-type and diffuse-type gastric cancers; primary central nervous system lymphomas and nodal diffuse large B-cell lymphomas; clear-cell renal cell carcinoma and papillary renal cell carcinoma; and different subtypes of liposarcoma.

26Furthermore, as a non-invasive, blood-based diagnostic tool, cell-free miRNAs have received much interest in recent years. Serum miR-145 has a distinct level in cancer patients compared with healthy ones, suggesting that detection of serum miR-145 has potential as a novel method for early cancer diagnosis,. Moreover, recent evidence has revealed that a combination of circulating miRNAs biomarkers show better sensitivity and specificity for cancer diagnosis. For example, in two independent studies, a combination of plasma markers miR-145 and miR-451, or a combination of miR-145, miR-155 and miR-382, were suggested to increase the sensitivity and specificity for discriminating breast cancer from healthy controls,. Likewise, circulating miR-145 combined with three other circulating miRNAs (miR-20a, miR-21 and miR-221) significantly identified aggressive prostate cancer patients, with an AUC of 0.824. Similarly, the combination of three plasma miRNAs (miR-21, miR-145 and miR-155) demonstrated strong potential as a diagnostic marker for early detection of lung cancer, with an AUC of 0.847. Moreover, cell-free miRNAs in other body excretions provide a novel approach for cancer diagnosis. The miR-145 level in urine was able to distinguish bladder cancer patients from non-cancer controls (77.8% sensitivity and 61.1% specificity for non-muscle invasive bladder cancer, AUC 0.729; and 84.1% and 61.1% for muscle invasive bladder cancer, respectively, AUC 0.790) and was significantly correlated with grade. Li et al. also explored the value of faecal miR-145 expression for colorectal cancer diagnosis.

27On the other hand, many reports have shown that miRNAs, including miR-145, are associated with the clinical outcome of human cancer patients. Time to relapse (TTR) was significantly shorter for NSCLC patients with low miR-145 expression compared with those with high levels. Furthermore, the combination of low miR-145 with p53 mutations was an independent marker of shorter TTR. In a study of 527 stage I NSCLC patients, low expression of miR-145 was correlated with brain metastasis. Huang et al. determined that down-regulation of miR-145 was associated with advanced stage and lymph node metastasis in small cell carcinoma of cervix. In addition, miR-145 expression levels in colorectal cancer were associated with tumour stage, depth of invasion (pT category), lymph node status (pN category), development of distant metastases, grade of tumour differentiation, maximal tumour diameter, anatomical localization and serum carcinoembryonic antigen levels, suggesting its potential role as a prognostic marker of colorectal cancer. In addition, miR-145 expression is able to predict the response of cancer cells to certain antitumour agents. For example, rectal cancer patients with a low intratumoural post-therapeutic expression of miR-145 had a significantly worse response to neoadjuvant therapy with 5-FU and 50.4 Gy radiation compared with those with high expression, suggesting miR-145 could serve as a response-predicting and prognostic marker in the course of neoadjuvant-treated colorectal cancer. Likewise, a profile of five serum miRNAs (miR-20a, miR-130, miR-145, miR-216 and miR-372) was identified as a biomarker to predict the chemosensitivity of colorectal cancer. However, in a study of 98 primary colorectal specimens, along with the corresponding normal mucosa specimens, miR-145 down-regulation had no relationship with other clinicopathological features, except the cancer site. Results from another group also found no outcome or clinicopathological relevance of miR-145 in colorectal cancer patients.

MiR-145 in cancer therapy

28The observation of decreased levels of tumour-suppressive miRNAs in cancers has led to the concept of miRNA replacement therapy. Recently, encouraging results have been achieved in several animal models –. A systemic or local application of a polyethylenimine-mediated delivery of unmodified miR-145 in a mouse model of colon carcinoma obtained a 40% or 60% decrease in tumour growth, respectively, with concomitant repression in ERK5 and c-Myc protein levels compared with negative controls. Moreover, delivery of miR-145 mimics by mesenchymal stem cells significantly decreased the migration of glioma cells and the self-renewal of germline stem cells.

29On the other hand, MiR-145 can influence the sensitivity of tumours to chemo-or radiation therapy, and a combination of miR-145 and chemo-or radiation therapy represents a novel antitumour strategy. Treatment with miR-145 inhibited gastric cancer cell growth and increased its sensitivity to 5-FU. Similarly, an adenoviral constructed miR-145 was injected into breast cancer orthotopic mouse models intratumourally, resulting in significant suppression of tumour growth. Furthermore, a treatment combining adenoviral miR-145 and 5-FU produced enhanced retardation of tumour growth, compared with treatment with either drug alone. In addition, miR-145 is able to enhance sensitivity to some molecular targeted drugs, including gefitinib and vemurafenib,. Ikemura et al. confirmed that MDR1 mRNA was a direct target of miR-145. However, further studies are still required to elucidate the mechanisms underlying the miR-145-mediated regulation of resistance to chemo-or radiotherapy.

Conclusions and future directions

30In summary, much evidence indicates that miR-145 represents a potent tumour suppressor, and aberrant miR-145 expression is found commonly in different cancers. Its tumour-suppressive function can be attributed to its regulation of target genes involved in multiple pathways, including proliferation, invasion, angiogenesis and CSCs. MiR-145 is closely associated with many signalling pathways; therefore, the discovery of novel targets is still required to obtain a comprehensive knowledge of the biological roles of miR-145.

31The close association between low expression of miR-145 and poor prognosis in cancer patients makes it a valuable prognostic biomarker. Moreover, its potential for cancer diagnosis has also been supported by many studies. More appealing is miR-145-based therapy. MiR-145 treatment can improve the sensitivity to chemotherapy agents in cancer cells, providing a new strategy for overcoming drug resistance. Furthermore, recent progress in drug-delivered systems provides a technical solution for the application of miRNA-based therapy to pre-clinical research. Currently, the application of specific miRNA mimics has demonstrated a great tumour-suppressive capacity in experimental tumour models, such as let-7 or miR-34 –. Research into miR-145-based therapy, however, is at an early stage, and effective delivery to the target tissues and drug safety remain challenges. Further investigation of miR-145 may lead to novel therapeutic strategies.

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Not in our library10.1038/nature03120
11.
Fukuda T, Yamagata K, Fujiyama S, et al. DEAD-box RNA helicase subunits of the Drosha complex are required for processing of rRNA and a subset of microRNAs. Nat Cell Biol. 2007;9:604-11.
Not in our library10.1038/ncb1577
12.
Yi R, Qin Y, Macara IG, et al. Exportin-5 mediates the nuclear export of pre-microRNAs and short hairpin RNAs. Genes Dev. 2003;17:3011-6.
Not in our library10.1101/gad.1158803
13.
Hutvagner G, McLachlan J, Pasquinelli AE, et al. A cellular function for the RNA-interference enzyme Dicer in the maturation of the let-7 small temporal RNA. Science. 2001;293:834-8.
Not in our library10.1126/science.1062961
14.
Ketting RF, Fischer SE, Bernstein E, et al. Dicer functions in RNA interference and in synthesis of small RNA involved in developmental timing in C. elegans. Genes Dev. 2001;15:2654-9.
Not in our library10.1101/gad.927801
15.
Haase AD, Jaskiewicz L, Zhang H, et al. TRBP, a regulator of cellular PKR and HIV-1 virus expression, interacts with Dicer and functions in RNA silencing. EMBO Rep. 2005;6:961-7.
Not in our library10.1038/sj.embor.7400509
16.
Chendrimada TP, Gregory RI, Kumaraswamy E, et al. TRBP recruits the Dicer complex to Ago2 for microRNA processing and gene silencing. Nature. 2005;436:740-4.
Not in our library10.1038/nature03868
17.
Cheloufi S, Dos Santos CO, Chong MM, et al. A dicer-independent miRNA biogenesis pathway that requires Ago catalysis. Nature. 2010;465:584-9.
Not in our library10.1038/nature09092
18.
Bartel DP. MicroRNAs: target recognition and regulatory functions. Cell. 2009;136:215-33.
Not in our library10.1016/j.cell.2009.01.002
19.
Liu X, Sempere LF, Galimberti F, et al. Uncovering growth-suppressive MicroRNAs in lung cancer. Clin Cancer Res. 2009;15:1177-83.
Not in our library10.1158/1078-0432.ccr-08-1355
20.
Cho WC, Chow AS, Au JS. Restoration of tumour suppressor hsa-miR-145 inhibits cancer cell growth in lung adenocarcinoma patients with epidermal growth factor receptor mutation. Eur J Cancer. 2009;45:2197-206.
Not in our library10.1016/j.ejca.2009.04.039
21.
Lehmann U, Streichert T, Otto B, et al. Identification of differentially expressed microRNAs in human male breast cancer. BMC Cancer. 2010;10:109.
Not in our library10.1186/1471-2407-10-109
22.
Radojicic J, Zaravinos A, Vrekoussis T, et al. MicroRNA expression analysis in triple-negative (ER, PR and Her2/neu) breast cancer. Cell Cycle. 2011;10:507-17.
Not in our library10.4161/cc.10.3.14754
23.
Iorio MV, Ferracin M, Liu CG, et al. MicroRNA gene expression deregulation in human breast cancer. Cancer Res. 2005;65:7065-70.
Not in our library10.1158/0008-5472.can-05-1783
24.
Sempere LF, Christensen M, Silahtaroglu A, et al. Altered MicroRNA expression confined to specific epithelial cell subpopulations in breast cancer. Cancer Res. 2007;67:11612-20.
Not in our library10.1158/0008-5472.can-07-5019
25.
Iorio MV, Visone R, Di Leva G, et al. MicroRNA signatures in human ovarian cancer. Cancer Res. 2007;67:8699-707.
Not in our library10.1158/0008-5472.can-07-1936
26.
Nam EJ, Yoon H, Kim SW, et al. MicroRNA expression profiles in serous ovarian carcinoma. Clin Cancer Res. 2008;14:2690-5.
Not in our library10.1158/1078-0432.ccr-07-1731
27.
Vaksman O, Stavnes HT, Kaern J, et al. miRNA profiling along tumour progression in ovarian carcinoma. J Cell Mol Med. 2011;15:1593-602.
Not in our library10.1111/j.1582-4934.2010.01148.x
28.
Porkka KP, Pfeiffer MJ, Waltering KK, et al. MicroRNA expression profiling in prostate cancer. Cancer Res. 2007;67:6130-5.
Not in our library10.1158/0008-5472.can-07-0533
29.
Ozen M, Creighton CJ, Ozdemir M, et al. Widespread deregulation of microRNA expression in human prostate cancer. Oncogene. 2008;27:1788-93.
Not in our library10.1038/sj.onc.1210809
30.
Schaefer A, Jung M, Mollenkopf HJ, et al. Diagnostic and prognostic implications of microRNA profiling in prostate carcinoma. Int J Cancer. 2010;126:1166-76.
Not in our library10.1002/ijc.24827
31.
Hart M, Nolte E, Wach S, et al. Comparative microRNA profiling of prostate carcinomas with increasing tumor stage by deep-sequencing. Mol Cancer Res. 2014;12:250-63.
Not in our library10.1158/1541-7786.mcr-13-0230
32.
Schepeler T, Reinert JT, Ostenfeld MS, et al. Diagnostic and prognostic microRNAs in stage II colon cancer. Cancer Res. 2008;68:6416-24.
Not in our library10.1158/0008-5472.can-07-6110
33.
Akao Y, Nakagawa Y, Naoe T. MicroRNAs 143 and 145 are possible common onco-microRNAs in human cancers. Oncol Rep. 2006;16:845-50.
Not in our library
34.
Identification by Real-time PCR of 13 mature microRNAs differentially expressed in colorectal cancer and non-tumoral tissues. · 2006
No notice
35.
Motoyama K, Inoue H, Takatsuno Y, et al. Over-and under-expressed microRNAs in human colorectal cancer. Int J Oncol. 2009;34:1069-75.
Not in our library10.3892/ijo_00000233
36.
Differential Expression of miRNAs in Colorectal Cancer: Comparison of Paired Tumor Tissue and Adjacent Normal Mucosa Using High-Throughput Sequencing · 2012
No notice
37.
Tan YG, Zhang YF, Guo CJ, et al. Screening of differentially expressed microRNA in ulcerative colitis related colorectal cancer. Asian Pac J Trop Med. 2013;6:972-6.
Not in our library10.1016/s1995-7645(13)60174-1
38.
Gramantieri L, Ferracin M, Fornari F, et al. Cyclin G1 is a target of miR-122a, a microRNA frequently down-regulated in human hepatocellular carcinoma. Cancer Res. 2007;67:6092-9.
Not in our library10.1158/0008-5472.can-06-4607
39.
Varnholt H, Drebber U, Schulze F, et al. MicroRNA gene expression profile of hepatitis C virus-associated hepatocellular carcinoma. Hepatology. 2008;47:1223-32.
Not in our library10.1002/hep.22158
40.
Gao P, Wong CC, Tung EK, et al. Deregulation of microRNA expression occurs early and accumulates in early stages of HBV-associated multistep hepatocarcinogenesis. J Hepatol. 2011;54:1177-84.
Not in our library10.1016/j.jhep.2010.09.023
41.
Jia Y, Liu H, Zhuang Q, et al. Tumorigenicity of cancer stem-like cells derived from hepatocarcinoma is regulated by microRNA-145. Oncol Rep. 2012;27:1865-72.
Not in our library10.3892/or.2012.1701
42.
Karakatsanis A, Papaconstantinou I, Gazouli M, et al. Expression of microRNAs, miR-21, miR-31, miR-122, miR-145, miR-146a, miR-200c, miR-221, miR-222, and miR-223 in patients with hepatocellular carcinoma or intrahepatic cholangiocarcinoma and its prognostic significance. Mol Carcinog. 2013;52:297-303.
Not in our library10.1002/mc.21864
43.
Real-Time PCR-Based Analysis of the Human Bile MicroRNAome Identifies miR-9 as a Potential Diagnostic Biomarker for Biliary Tract Cancer · 2011
No notice
44.
Cao P, Zhou L, Zhang J, et al. Comprehensive expression profiling of microRNAs in laryngeal squamous cell carcinoma. Head Neck. 2013;35:720-8.
Not in our library10.1002/hed.23011
45.
Wijnhoven BP, Hussey DJ, Watson DI, et al. MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma. Br J Surg. 2010;97:853-61.
Not in our library10.1002/bjs.7000
46.
Wu BL, Xu LY, Du ZP, et al. MiRNA profile in esophageal squamous cell carcinoma: downregulation of miR-143 and miR-145. World J Gastroenterol. 2011;17:79-88.
Not in our library10.3748/wjg.v17.i1.79
47.
Zhu L, Yan W, Rodriguez-Canales J, et al. MicroRNA analysis of microdissected normal squamous esophageal epithelium and tumor cells. Am J Cancer Res. 2011;1:574-84.
Not in our library
48.
Gu J, Wang Y, Wu X. MicroRNA in the pathogenesis and prognosis of esophageal cancer. Curr Pharm Des. 2013;19:1292-300.
Not in our library10.2174/138161213804805775
49.
Papaconstantinou IG, Manta A, Gazouli M, et al. Expression of microRNAs in patients with pancreatic cancer and its prognostic significance. Pancreas. 2013;42:67-71.
Not in our library10.1097/mpa.0b013e3182592ba7
50.
Yu T, Wang XY, Gong RG, et al. The expression profile of microRNAs in a model of 7,12-dimethyl-benz[a]anthrance-induced oral carcinogenesis in Syrian hamster. J Exp Clin Cancer Res. 2009;28:64.
Not in our library10.1186/1756-9966-28-64
51.
Gao L, Ren W, Chang S, et al. Downregulation of miR-145 expression in oral squamous cell carcinomas and its clinical significance. Onkologie. 2013;36:194-9.
Not in our library10.1159/000349956
52.
Ichimi T, Enokida H, Okuno Y, et al. Identification of novel microRNA targets based on microRNA signatures in bladder cancer. Int J Cancer. 2009;125:345-52.
Not in our library10.1002/ijc.24390
53.
Song T, Xia W, Shao N, et al. Differential miRNA expression profiles in bladder urothelial carcinomas. Asian Pac J Cancer Prev. 2010;11:905-11.
Not in our library
54.
Pignot G, Cizeron-Clairac G, Vacher S, et al. microRNA expression profile in a large series of bladder tumors: identification of a 3-miRNA signature associated with aggressiveness of muscle-invasive bladder cancer. Int J Cancer. 2013;132:2479-91.
Not in our library10.1002/ijc.27949
55.
Ratert N, Meyer HA, Jung M, et al. miRNA profiling identifies candidate mirnas for bladder cancer diagnosis and clinical outcome. J Mol Diagn. 2013;15:695-705.
Not in our library10.1016/j.jmoldx.2013.05.008
56.
Dip N, Reis ST, Srougi M, et al. Expression profile of microrna-145 in urothelial bladder cancer. Int Braz J Urol. 2013;39:95-101.
Not in our library10.1590/s1677-5538.ibju.2013.01.12
57.
Zaravinos A, Radojicic J, Lambrou GI, et al. Expression of miRNAs involved in angiogenesis, tumor cell proliferation, tumor suppressor inhibition, epithelial-mesenchymal transition and activation of metastasis in bladder cancer. J Urol. 2012;188:615-23.
Not in our library10.1016/j.juro.2012.03.122
58.
MicroRNA deregulation and pathway alterations in nasopharyngeal carcinoma · 2009
No notice
59.
Haapa-Paananen S, Chen P, Hellstrom K, et al. Functional profiling of precursor MicroRNAs identifies MicroRNAs essential for glioma proliferation. PLoS ONE. 2013;8:e60930.
Not in our library10.1371/journal.pone.0060930
60.
Sand M, Skrygan M, Georgas D, et al. Microarray analysis of microRNA expression in cutaneous squamous cell carcinoma. J Dermatol Sci. 2012;68:119-26.
Not in our library10.1016/j.jdermsci.2012.09.004
61.
Sand M, Skrygan M, Sand D, et al. Expression of microRNAs in basal cell carcinoma. Br J Dermatol. 2012;167:847-55.
Not in our library10.1111/j.1365-2133.2012.11022.x
62.
Gits CM, van Kuijk PF, Jonkers MB, et al. Microrna expression profiles distinguish liposarcoma subtypes and implicate MIR-145 AND MIR-451 as tumor suppressors. Int J Cancer. 2014;135:348-61.
Not in our library10.1002/ijc.28694
63.
Akao Y, Nakagawa Y, Kitade Y, et al. Downregulation of microRNAs-143 and-145 in B-cell malignancies. Cancer Sci. 2007;98:1914-20.
Not in our library10.1111/j.1349-7006.2007.00618.x
64.
Hermeking H. p53 enters the microRNA world. Cancer Cell. 2007;12:414-8.
Not in our library10.1016/j.ccr.2007.10.028
65.
Barlev NA, Sayan BS, Candi E, et al. The microRNA and p53 families join forces against cancer. Cell Death Differ. 2010;17:373-5.
Not in our library10.1038/cdd.2009.73
66.
Sachdeva M, Zhu S, Wu F, et al. p53 represses c-Myc through induction of the tumor suppressor miR-145. Proc Natl Acad Sci USA. 2009;106:3207-12.
Not in our library10.1073/pnas.0808042106
67.
Suh SO, Chen Y, Zaman MS, et al. MicroRNA-145 is regulated by DNA methylation and p53 gene mutation in prostate cancer. Carcinogenesis. 2011;32:772-8.
Not in our library10.1093/carcin/bgr036
68.
Shi M, Du L, Liu D, et al. Glucocorticoid regulation of a novel HPV-E6-p53-miR-145 pathway modulates invasion and therapy resistance of cervical cancer cells. J Pathol. 2012;228:148-57.
Not in our library10.1002/path.3997
69.
Ren D, Wang M, Guo W, et al. Wild-type p53 suppresses the epithelial-mesenchymal transition and stemness in PC-3 prostate cancer cells by modulating miR145. Int J Oncol. 2013;42:1473-81.
Not in our library10.3892/ijo.2013.1825
70.
Spizzo R, Nicoloso MS, Lupini L, et al. miR-145 participates with TP53 in a death-promoting regulatory loop and targets estrogen receptor-alpha in human breast cancer cells. Cell Death Differ. 2010;17:246-54.
Not in our library10.1038/cdd.2009.117
71.
Suzuki HI, Yamagata K, Sugimoto K, et al. Modulation of microRNA processing by p53. Nature. 2009;460:529-33.
Not in our library10.1038/nature08199
72.
Zhang J, Sun Q, Zhang Z, et al. Loss of microRNA-143/145 disturbs cellular growth and apoptosis of human epithelial cancers by impairing the MDM2-p53 feedback loop. Oncogene. 2013;32:61-9.
Not in our library10.1038/onc.2012.28
73.
Hingorani SR, Tuveson DA. Ras redux: rethinking how and where Ras acts. Curr Opin Genet Dev. 2003;13:6-13.
Not in our library10.1016/s0959-437x(02)00017-5
74.
Kent OA, Chivukula RR, Mullendore M, et al. Repression of the miR-143/145 cluster by oncogenic Ras initiates a tumor-promoting feed-forward pathway. Genes Dev. 2010;24:2754-9.
Not in our library10.1101/gad.1950610
75.
Kent OA, Fox-Talbot K, Halushka MK. RREB1 repressed miR-143/145 modulates KRAS signaling through downregulation of multiple targets. Oncogene. 2013;32:2576-85.
Not in our library10.1038/onc.2012.266
76.
Mosakhani N, Sarhadi VK, Borze I, et al. MicroRNA profiling differentiates colorectal cancer according to KRAS status. Genes Chromosom Cancer. 2012;51:1-9.
Not in our library10.1002/gcc.20925
77.
Sachdeva M, Liu Q, Cao J, et al. Negative regulation of miR-145 by C/EBP-beta through the Akt pathway in cancer cells. Nucleic Acids Res. 2012;40:6683-92.
Not in our library10.1093/nar/gks324
78.
Gan B, Lim C, Chu G, et al. FoxOs enforce a progression checkpoint to constrain mTORC1-activated renal tumorigenesis. Cancer Cell. 2010;18:472-84.
Not in our library10.1016/j.ccr.2010.10.019
79.
Schepeler T, Holm A, Halvey P, et al. Attenuation of the beta-catenin/TCF4 complex in colorectal cancer cells induces several growth-suppressive microRNAs that target cancer promoting genes. Oncogene. 2012;31:2750-60.
Not in our library10.1038/onc.2011.453
80.
Kawai S, Amano A. BRCA1 regulates microRNA biogenesis via the DROSHA microprocessor complex. J Cell Biol. 2012;197:201-8.
Not in our library10.1083/jcb.201110008
81.
Hong S, Noh H, Chen H, et al. Signaling by p38 MAPK stimulates nuclear localization of the microprocessor component p68 for processing of selected primary microRNAs. Sci Signal. 2013;6:ra16.
Not in our library10.1126/scisignal.2003706
82.
Xhemalce B, Robson SC, Kouzarides T. Human RNA methyltransferase BCDIN3D regulates microRNA processing. Cell. 2012;151:278-88.
Not in our library10.1016/j.cell.2012.08.041
83.
Iio A, Takagi T, Miki K, et al. DDX6 post-transcriptionally down-regulates miR-143/145 expression through host gene NCR143/145 in cancer cells. Biochim Biophys Acta. 2013;1829:1102-10.
Not in our library10.1016/j.bbagrm.2013.07.010
84.
DCLK1 Regulates Pluripotency and Angiogenic Factors via microRNA-Dependent Mechanisms in Pancreatic Cancer · 2013
No notice
85.
Shi B, Sepp-Lorenzino L, Prisco M, et al. Micro RNA 145 targets the insulin receptor substrate-1 and inhibits the growth of colon cancer cells. J Biol Chem. 2007;282:32582-90.
Not in our library10.1074/jbc.m702806200
86.
La Rocca G, Badin M, Shi B, et al. Mechanism of growth inhibition by MicroRNA 145: the role of the IGF-I receptor signaling pathway. J Cell Physiol. 2009;220:485-91.
Not in our library10.1002/jcp.21796
87.
Cho WC, Chow AS, Au JS. MiR-145 inhibits cell proliferation of human lung adenocarcinoma by targeting EGFR and NUDT1. RNA Biol. 2011;8:125-31.
Not in our library10.4161/rna.8.1.14259
88.
Zhang J, Guo H, Qian G, et al. MiR-145, a new regulator of the DNA fragmentation factor-45 (DFF45)-mediated apoptotic network. Mol Cancer. 2010;9:211.
Not in our library10.1186/1476-4598-9-211
89.
Ostenfeld MS, Bramsen JB, Lamy P, et al. miR-145 induces caspase-dependent and-independent cell death in urothelial cancer cell lines with targeting of an expression signature present in Ta bladder tumors. Oncogene. 2010;29:1073-84.
Not in our library10.1038/onc.2009.395
90.
Sachdeva M, Mo YY. MicroRNA-145 suppresses cell invasion and metastasis by directly targeting mucin 1. Cancer Res. 2010;70:378-87.
Not in our library10.1158/0008-5472.can-09-2021
91.
Fuse M, Nohata N, Kojima S, et al. Restoration of miR-145 expression suppresses cell proliferation, migration and invasion in prostate cancer by targeting FSCN1. Int J Oncol. 2011;38:1093-101.
Not in our library10.3892/ijo.2011.919
92.
Speranza MC, Frattini V, Pisati F, et al. NEDD9, a novel target of miR-145, increases the invasiveness of glioblastoma. Oncotarget. 2012;3:723-34.
Not in our library10.18632/oncotarget.547
93.
Yu CC, Tsai LL, Wang ML, et al. miR145 targets the SOX9/ADAM17 axis to inhibit tumor-initiating cells and IL-6-mediated paracrine effects in head and neck cancer. Cancer Res. 2013;73:3425-40.
Not in our library10.1158/0008-5472.can-12-3840
94.
Xu N, Papagiannakopoulos T, Pan G, et al. MicroRNA-145 regulates OCT4, SOX2, and KLF4 and represses pluripotency in human embryonic stem cells. Cell. 2009;137:647-58.
Not in our library10.1016/j.cell.2009.02.038
95.
Hu J, Guo H, Li H, et al. MiR-145 regulates epithelial to mesenchymal transition of breast cancer cells by targeting Oct4. PLoS ONE. 2012;7:e45965.
Not in our library10.1371/journal.pone.0045965
96.
Fan L, Wu Q, Xing X, et al. MicroRNA-145 targets vascular endothelial growth factor and inhibits invasion and metastasis of osteosarcoma cells. Acta Biochim Biophys Sin (Shanghai). 2012;44:407-14.
Not in our library10.1093/abbs/gms019
97.
Xu Q, Liu LZ, Qian X, et al. MiR-145 directly targets p70S6K1 in cancer cells to inhibit tumor growth and angiogenesis. Nucleic Acids Res. 2012;40:761-74.
Not in our library10.1093/nar/gkr730
98.
Zou C, Xu Q, Mao F, et al. MiR-145 inhibits tumor angiogenesis and growth by N-RAS and VEGF. Cell Cycle. 2012;11:2137-45.
Not in our library10.4161/cc.20598
99.
Lee CY, Rennie PS, Jia WW. MicroRNA regulation of oncolytic herpes simplex virus-1 for selective killing of prostate cancer cells. Clin Cancer Res. 2009;15:5126-35.
Not in our library10.1158/1078-0432.ccr-09-0051
100.
Aberrant Expression of Oncogenic and Tumor-Suppressive MicroRNAs in Cervical Cancer Is Required for Cancer Cell Growth · 2008
No notice
101.
Xing AY, Wang B, Shi DB, et al. Deregulated expression of miR-145 in manifold human cancer cells. Exp Mol Pathol. 2013;95:91-7.
Not in our library10.1016/j.yexmp.2013.05.003
102.
Law PT, Ching AK, Chan AW, et al. MiR-145 modulates multiple components of the insulin-like growth factor pathway in hepatocellular carcinoma. Carcinogenesis. 2012;33:1134-41.
Not in our library10.1093/carcin/bgs130
103.
Zhu H, Dougherty U, Robinson V, et al. EGFR signals downregulate tumor suppressors miR-143 and miR-145 in Western diet-promoted murine colon cancer: role of G1 regulators. Mol Cancer Res. 2011;9:960-75.
Not in our library10.1158/1541-7786.mcr-10-0531
104.
Zhong M, Ma X, Sun C, et al. MicroRNAs reduce tumor growth and contribute to enhance cytotoxicity induced by gefitinib in non-small cell lung cancer. Chem Biol Interact. 2010;184:431-8.
Not in our library10.1016/j.cbi.2010.01.025
105.
Noguchi S, Yasui Y, Iwasaki J, et al. Replacement treatment with microRNA-143 and-145 induces synergistic inhibition of the growth of human bladder cancer cells by regulating PI3K/Akt and MAPK signaling pathways. Cancer Lett. 2013;328:353-61.
Not in our library10.1016/j.canlet.2012.10.017
106.
Sudbery I, Enright AJ, Fraser AG, et al. Systematic analysis of off-target effects in an RNAi screen reveals microRNAs affecting sensitivity to TRAIL-induced apoptosis. BMC Genomics. 2010;11:175.
Not in our library10.1186/1471-2164-11-175
107.
The functional significance of microRNA-145 in prostate cancer · 2010
Corrected
108.
Noguchi S, Yamada N, Kumazaki M, et al. socs7, a target gene of microRNA-145, regulates interferon-beta induction through STAT3 nuclear translocation in bladder cancer cells. Cell Death Dis. 2013;4:e482.
Not in our library10.1038/cddis.2013.11
109.
miRNA-145 inhibits non-small cell lung cancer cell proliferation by targeting c-Myc · 2010
No notice
110.
Seoane J, Le HV, Massague J. Myc suppression of the p21(Cip1) Cdk inhibitor influences the outcome of the p53 response to DNA damage. Nature. 2002;419:729-34.
Not in our library10.1038/nature01119
111.
Zhang W, Wang Q, Yu M, et al. MicroRNA-145 function as a cell growth repressor by directly targeting c-Myc in human ovarian cancer. Technol Cancer Res Treat. 2014;13:161-8.
Not in our library10.7785/tcrt.2012.500367
112.
Kim SJ, Oh JS, Shin JY, et al. Development of microRNA-145 for therapeutic application in breast cancer. J Control Release. 2011;155:427-34.
Not in our library10.1016/j.jconrel.2011.06.026
113.
Wang F, Xia J, Wang N, et al. miR-145 inhibits proliferation and invasion of esophageal squamous cell carcinoma in part by targeting c-Myc. Onkologie. 2013;36:754-8.
Not in our library10.1159/000356978
114.
Shao Y, Qu Y, Dang S, et al. MiR-145 inhibits oral squamous cell carcinoma (OSCC) cell growth by targeting c-Myc and Cdk6. Cancer Cell Int. 2013;13:51.
Not in our library10.1186/1475-2867-13-51
115.
Seth A, Watson DK. ETS transcription factors and their emerging roles in human cancer. Eur J Cancer. 2005;41:2462-78.
Not in our library10.1016/j.ejca.2005.08.013
116.
Zhang J, Guo H, Zhang H, et al. Putative tumor suppressor miR-145 inhibits colon cancer cell growth by targeting oncogene Friend leukemia virus integration 1 gene. Cancer. 2011;117:86-95.
Not in our library10.1002/cncr.25522
117.
Hart M, Wach S, Nolte E, et al. The proto-oncogene ERG is a target of microRNA miR-145 in prostate cancer. FEBS J. 2013;280:2105-16.
Not in our library10.1111/febs.12236
118.
Zheng L, Pu J, Qi T, et al. miRNA-145 targets v-ets erythroblastosis virus E26 oncogene homolog 1 to suppress the invasion, metastasis, and angiogenesis of gastric cancer cells. Mol Cancer Res. 2013;11:182-93.
Not in our library10.1158/1541-7786.mcr-12-0534
119.
Kovar H. Downstream EWS/FLI1-upstream Ewing's sarcoma. Genome Med. 2010;2:8.
Not in our library10.1186/gm129
120.
Ban J, Jug G, Mestdagh P, et al. Hsa-mir-145 is the top EWS-FLI1-repressed microRNA involved in a positive feedback loop in Ewing's sarcoma. Oncogene. 2011;30:2173-80.
Not in our library10.1038/onc.2010.581
121.
Miles GD, Seiler M, Rodriguez L, et al. Identifying microRNA/mRNA dysregulations in ovarian cancer. BMC Res Notes. 2012;5:164.
Not in our library10.1186/1756-0500-5-164
122.
Wang S, Bian C, Yang Z, et al. miR-145 inhibits breast cancer cell growth through RTKN. Int J Oncol. 2009;34:1461-6.
Not in our library
123.
MicroRNA-145 Targets YES and STAT1 in Colon Cancer Cells · 2010
No notice
124.
Noh JH, Chang YG, Kim MG, et al. MiR-145 functions as a tumor suppressor by directly targeting histone deacetylase 2 in liver cancer. Cancer Lett. 2013;335:455-62.
Not in our library10.1016/j.canlet.2013.03.003
125.
Villadsen SB, Bramsen JB, Ostenfeld MS, et al. The miR-143/-145 cluster regulates plasminogen activator inhibitor-1 in bladder cancer. Br J Cancer. 2012;106:366-74.
Not in our library10.1038/bjc.2011.520
126.
Tchernitsa O, Kasajima A, Schafer R, et al. Systematic evaluation of the miRNA-ome and its downstream effects on mRNA expression identifies gastric cancer progression. J Pathol. 2010;222:310-9.
Not in our library10.1002/path.2759
127.
Leite KR, Tomiyama A, Reis ST, et al. MicroRNA expression profiles in the progression of prostate cancer–from high-grade prostate intraepithelial neoplasia to metastasis. Urol Oncol. 2013;31:796-801.
Not in our library10.1016/j.urolonc.2011.07.002
128.
Shao Y, Zhang SQ, Quan F, et al. MicroRNA-145 inhibits the proliferation, migration and invasion of the human TCA8113 oral cancer line. Oncol Lett. 2013;6:1636-40.
Not in our library10.3892/ol.2013.1621
129.
Baldus SE, Monig SP, Huxel S, et al. MUC1 and nuclear beta-catenin are coexpressed at the invasion front of colorectal carcinomas and are both correlated with tumor prognosis. Clin Cancer Res. 2004;10:2790-6.
Not in our library10.1158/1078-0432.ccr-03-0163
130.
Schroeder JA, Adriance MC, Thompson MC, et al. MUC1 alters beta-catenin-dependent tumor formation and promotes cellular invasion. Oncogene. 2003;22:1324-32.
Not in our library10.1038/sj.onc.1206291
131.
Sachdeva M, Mo YY. miR-145-mediated suppression of cell growth, invasion and metastasis. Am J Transl Res. 2010;2:170-80.
Not in our library
132.
Wu H, Xiao Z, Wang K, et al. MiR-145 is downregulated in human ovarian cancer and modulates cell growth and invasion by targeting p70S6K1 and MUC1. Biochem Biophys Res Commun. 2013;441:693-700.
Not in our library10.1016/j.bbrc.2013.10.053
133.
Dynoodt P, Speeckaert R, De Wever O, et al. miR-145 overexpression suppresses the migration and invasion of metastatic melanoma cells. Int J Oncol. 2013;42:1443-51.
Not in our library10.3892/ijo.2013.1823
134.
miR-145 and miR-133a function as tumour suppressors and directly regulate FSCN1 expression in bladder cancer · 2010
No notice
135.
Kano M, Seki N, Kikkawa N, et al. miR-145, miR-133a and miR-133b: tumor-suppressive miRNAs target FSCN1 in esophageal squamous cell carcinoma. Int J Cancer. 2010;127:2804-14.
Not in our library10.1002/ijc.25284
136.
Liu R, Liao J, Yang M, et al. The cluster of miR-143 and miR-145 affects the risk for esophageal squamous cell carcinoma through co-regulating fascin homolog 1. PLoS ONE. 2012;7:e33987.
Not in our library10.1371/journal.pone.0033987
137.
Gotte M, Mohr C, Koo CY, et al. miR-145-dependent targeting of junctional adhesion molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness. Oncogene. 2010;29:6569-80.
Not in our library10.1038/onc.2010.386
138.
Noguchi S, Mori T, Hoshino Y, et al. Comparative study of anti-oncogenic microRNA-145 in canine and human malignant melanoma. J Vet Med Sci. 2012;74:1-8.
Not in our library10.1292/jvms.11-0264
139.
Chiyomaru T, Tatarano S, Kawakami K, et al. SWAP70, actin-binding protein, function as an oncogene targeting tumor-suppressive miR-145 in prostate cancer. Prostate. 2011.
Not in our library10.1002/pros.21372
140.
Tikhmyanova N, Golemis EA. NEDD9 and BCAR1 negatively regulate E-cadherin membrane localization, and promote E-cadherin degradation. PLoS ONE. 2011;6:e22102.
Not in our library10.1371/journal.pone.0022102
141.
O'Neill GM, Seo S, Serebriiskii IG, et al. A new central scaffold for metastasis: parsing HEF1/Cas-L/NEDD9. Cancer Res. 2007;67:8975-9.
Not in our library10.1158/0008-5472.can-07-1328
142.
Guo W, Ren D, Chen X, et al. HEF1 promotes epithelial mesenchymal transition and bone invasion in prostate cancer under the regulation of microRNA-145. J Cell Biochem. 2013;114:1606-15.
Not in our library10.1002/jcb.24502
143.
Lu R, Ji Z, Li X, et al. miR-145 functions as tumor suppressor and targets two oncogenes, ANGPT2 and NEDD9, in renal cell carcinoma. J Cancer Res Clin Oncol. 2014;140:387-97.
Not in our library10.1007/s00432-013-1577-z
144.
Gao P, Xing AY, Zhou GY, et al. The molecular mechanism of microRNA-145 to suppress invasion-metastasis cascade in gastric cancer. Oncogene. 2013;32:491-501.
Not in our library10.1038/onc.2012.61
145.
Rani SB, Rathod SS, Karthik S, et al. MiR-145 functions as a tumor-suppressive RNA by targeting Sox9 and adducin 3 in human glioma cells. Neuro Oncol. 2013;15:1302-16.
Not in our library10.1093/neuonc/not090
146.
Mochizuki S, Okada Y. ADAMs in cancer cell proliferation and progression. Cancer Sci. 2007;98:621-8.
Not in our library10.1111/j.1349-7006.2007.00434.x
147.
Doberstein K, Steinmeyer N, Hartmetz AK, et al. MicroRNA-145 targets the metalloprotease ADAM17 and is suppressed in renal cell carcinoma patients. Neoplasia. 2013;15:218-30.
Not in our library10.1593/neo.121222
148.
Lu Y, Chopp M, Zheng X, et al. MiR-145 reduces ADAM17 expression and inhibits in vitro migration and invasion of glioma cells. Oncol Rep. 2013;29:67-72.
Not in our library10.3892/or.2012.2084
149.
Lee HK, Bier A, Cazacu S, et al. MicroRNA-145 is downregulated in glial tumors and regulates glioma cell migration by targeting connective tissue growth factor. PLoS ONE. 2013;8:e54652.
Not in our library10.1371/journal.pone.0054652
150.
Yamada N, Noguchi S, Mori T, et al. Tumor-suppressive microRNA-145 targets catenin delta-1 to regulate Wnt/beta-catenin signaling in human colon cancer cells. Cancer Lett. 2013;335:332-42.
Not in our library10.1016/j.canlet.2013.02.060
151.
Wang Z, Zhang X, Yang Z, et al. MiR-145 regulates PAK4 via the MAPK pathway and exhibits an antitumor effect in human colon cells. Biochem Biophys Res Commun. 2012;427:444-9.
Not in our library10.1016/j.bbrc.2012.06.123
152.
Characterization of global microRNA expression reveals oncogenic potential of miR-145 in metastatic colorectal cancer · 2009
No notice
153.
Koo S, Martin GS, Schulz KJ, et al. Serial selection for invasiveness increases expression of miR-143/miR-145 in glioblastoma cell lines. BMC Cancer. 2012;12:143.
Not in our library10.1186/1471-2407-12-143
154.
Dean M, Fojo T, Bates S. Tumour stem cells and drug resistance. Nat Rev Cancer. 2005;5:275-84.
Not in our library10.1038/nrc1590
155.
Biddle A, Mackenzie IC. Cancer stem cells and EMT in carcinoma. Cancer Metastasis Rev. 2012;31:285-93.
Not in our library10.1007/s10555-012-9345-0
156.
Takahashi K, Yamanaka S. Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell. 2006;126:663-76.
Not in our library10.1016/j.cell.2006.07.024
157.
Takahashi K, Tanabe K, Ohnuki M, et al. Induction of pluripotent stem cells from adult human fibroblasts by defined factors. Cell. 2007;131:861-72.
Not in our library10.1016/j.cell.2007.11.019
158.
Yu J, Vodyanik MA, Smuga-Otto K, et al. Induced pluripotent stem cell lines derived from human somatic cells. Science. 2007;318:1917-20.
Not in our library10.1126/science.1151526
159.
The SOX2 response program in glioblastoma multiforme: an integrated ChIP-seq, expression microarray, and microRNA analysis · 2011
No notice
160.
Wu Y, Liu S, Xin H, et al. Up-regulation of microRNA-145 promotes differentiation by repressing OCT4 in human endometrial adenocarcinoma cells. Cancer. 2011;117:3989-98.
Not in our library10.1002/cncr.25944
161.
Yin R, Zhang S, Wu Y, et al. microRNA-145 suppresses lung adenocarcinoma-initiating cell proliferation by targeting OCT4. Oncol Rep. 2011;25:1747-54.
Not in our library10.3892/or.2011.1252
162.
Polytarchou C, Iliopoulos D, Struhl K. An integrated transcriptional regulatory circuit that reinforces the breast cancer stem cell state. Proc Natl Acad Sci USA. 2012;109:14470-5.
Not in our library10.1073/pnas.1212811109
163.
Huang S, Guo W, Tang Y, et al. miR-143 and miR-145 inhibit stem cell characteristics of PC-3 prostate cancer cells. Oncol Rep. 2012;28:1831-7.
Not in our library10.3892/or.2012.2015
164.
Holmgren L, O'Reilly MS, Folkman J. Dormancy of micrometastases: balanced proliferation and apoptosis in the presence of angiogenesis suppression. Nat Med. 1995;1:149-53.
Not in our library10.1038/nm0295-149
165.
Yin Y, Yan ZP, Lu NN, et al. Downregulation of miR-145 associated with cancer progression and VEGF transcriptional activation by targeting N-RAS and IRS1. Biochim Biophys Acta. 2013;1829:239-47.
Not in our library10.1016/j.bbagrm.2012.11.006
166.
Lajer CB, Garnaes E, Friis-Hansen L, et al. The role of miRNAs in human papilloma virus (HPV)-associated cancers: bridging between HPV-related head and neck cancer and cervical cancer. Br J Cancer. 2012;106:1526-34.
Not in our library10.1038/bjc.2012.109
167.
Chinnathambi S, Wiechert S, Tomanek-Chalkley A, et al. Treatment with the cancer drugs decitabine and doxorubicin induces human skin keratinocytes to express Oct4 and the OCT4 regulator mir-145. J Dermatol. 2012;39:617-24.
Not in our library10.1111/j.1346-8138.2012.01553.x
168.
Bockmeyer CL, Christgen M, Muller M, et al. MicroRNA profiles of healthy basal and luminal mammary epithelial cells are distinct and reflected in different breast cancer subtypes. Breast Cancer Res Treat. 2011;130:735-45.
Not in our library10.1007/s10549-010-1303-3
169.
Wach S, Nolte E, Szczyrba J, et al. MicroRNA profiles of prostate carcinoma detected by multiplatform microRNA screening. Int J Cancer. 2012;130:611-21.
Not in our library10.1002/ijc.26064
170.
Li X, Luo F, Li Q, et al. Identification of new aberrantly expressed miRNAs in intestinal-type gastric cancer and its clinical significance. Oncol Rep. 2011;26:1431-9.
Not in our library10.3892/or.2011.1437
171.
Fischer L, Hummel M, Korfel A, et al. Differential micro-RNA expression in primary CNS and nodal diffuse large B-cell lymphomas. Neuro Oncol. 2011;13:1090-8.
Not in our library10.1093/neuonc/nor107
172.
Wach S, Nolte E, Theil A, et al. MicroRNA profiles classify papillary renal cell carcinoma subtypes. Br J Cancer. 2013;109:714-22.
Not in our library10.1038/bjc.2013.313
173.
Chung YW, Bae HS, Song JY, et al. Detection of microRNA as novel biomarkers of epithelial ovarian cancer from the serum of ovarian cancer patient. Int J Gynecol Cancer. 2013;23:673-9.
Not in our library10.1097/igc.0b013e31828c166d
174.
Circulating microRNAs in breast cancer and healthy subjects · 2009
No notice
175.
Mar-Aguilar F, Mendoza-Ramirez JA, Malagon-Santiago I, et al. Serum circulating microRNA profiling for identification of potential breast cancer biomarkers. Dis Markers. 2013;34:163-9.
Not in our library10.3233/dma-120957
176.
Circulating microRNAs as Specific Biomarkers for Breast Cancer Detection · 2013
No notice
177.
Shen J, Hruby GW, McKiernan JM, et al. Dysregulation of circulating microRNAs and prediction of aggressive prostate cancer. Prostate. 2012;72:1469-77.
Not in our library10.1002/pros.22499
178.
Tang D, Shen Y, Wang M, et al. Identification of plasma microRNAs as novel noninvasive biomarkers for early detection of lung cancer. Eur J Cancer Prev. 2013;22:540-8.
Not in our library10.1097/cej.0b013e32835f3be9
179.
Yun SJ, Jeong P, Kim WT, et al. Cell-free microRNAs in urine as diagnostic and prognostic biomarkers of bladder cancer. Int J Oncol. 2012;41:1871-8.
Not in our library10.3892/ijo.2012.1622
180.
Li JM, Zhao RH, Li ST, et al. Down-regulation of fecal miR-143 and miR-145 as potential markers for colorectal cancer. Saudi Med J. 2012;33:24-9.
Not in our library
181.
Campayo M, Navarro A, Vinolas N, et al. Low miR-145 and high miR-367 are associated with unfavourable prognosis in resected nonsmall cell lung cancer. Eur Respir J. 2013;41:1172-8.
Not in our library10.1183/09031936.00048712
182.
Lu Y, Govindan R, Wang L, et al. MicroRNA profiling and prediction of recurrence/relapse-free survival in stage I lung cancer. Carcinogenesis. 2012;33:1046-54.
Not in our library10.1093/carcin/bgs100
183.
Downregulation of six microRNAs is associated with advanced stage, lymph node metastasis and poor prognosis in small cell carcinoma of the cervix. · 2012
Not checked
184.
Slaby O, Svoboda M, Fabian P, et al. Altered expression of miR-21, miR-31, miR-143 and miR-145 is related to clinicopathologic features of colorectal cancer. Oncology. 2007;72:397-402.
Not in our library10.1159/000113489
185.
Drebber U, Lay M, Wedemeyer I, et al. Altered levels of the onco-microRNA 21 and the tumor-supressor microRNAs 143 and 145 in advanced rectal cancer indicate successful neoadjuvant chemoradiotherapy. Int J Oncol. 2011;39:409-15.
Not in our library10.3892/ijo.2011.1036
186.
Zhang J, Zhang K, Bi M, et al. Circulating microRNA expressions in colorectal cancer as predictors of response to chemotherapy. Anticancer Drugs. 2014;25:346-52.
Not in our library10.1097/cad.0000000000000049
187.
Wang CJ, Zhou ZG, Wang L, et al. Clinicopathological significance of microRNA-31,-143 and-145 expression in colorectal cancer. Dis Markers. 2009;26:27-34.
Not in our library10.3233/dma-2009-0601
188.
Clinical relevance of microRNA miR-21, miR-31, miR-92a, miR-101, miR-106a and miR-145 in colorectal cancer · 2012
No notice
189.
Takeshita F, Patrawala L, Osaki M, et al. Systemic delivery of synthetic microRNA-16 inhibits the growth of metastatic prostate tumors via downregulation of multiple cell-cycle genes. Mol Ther. 2010;18:181-7.
Not in our library10.1038/mt.2009.207
190.
Kumar MS, Erkeland SJ, Pester RE, et al. Suppression of non-small cell lung tumor development by the let-7 microRNA family. Proc Natl Acad Sci USA. 2008;105:3903-8.
Not in our library10.1073/pnas.0712321105
191.
Kota J, Chivukula RR, O'Donnell KA, et al. Therapeutic microRNA delivery suppresses tumorigenesis in a murine liver cancer model. Cell. 2009;137:1005-17.
Not in our library10.1016/j.cell.2009.04.021
192.
Ibrahim AF, Weirauch U, Thomas M, et al. MicroRNA replacement therapy for miR-145 and miR-33a is efficacious in a model of colon carcinoma. Cancer Res. 2011;71:5214-24.
Not in our library10.1158/0008-5472.can-10-4645
193.
Mesenchymal stem cells deliver synthetic microRNA mimics to glioma cells and glioma stem cells and inhibit their cell migration and self-renewal · 2013
No notice
194.
Takagi T, Iio A, Nakagawa Y, et al. Decreased expression of microRNA-143 and-145 in human gastric cancers. Oncology. 2009;77:12-21.
Not in our library10.1159/000218166
195.
Peng W, Hu J, Zhu XD, et al. Overexpression of miR-145 increases the sensitivity of vemurafenib in drug-resistant colo205 cell line. Tumour Biol. 2014;35:2983-8.
Not in our library10.1007/s13277-013-1383-x
196.
Ikemura K, Yamamoto M, Miyazaki S, et al. MicroRNA-145 post-transcriptionally regulates the expression and function of P-glycoprotein in intestinal epithelial cells. Mol Pharmacol. 2013;83:399-405.
Not in our library10.1124/mol.112.081844

Cited by papers we hold 1

Whole genome sequencing puts forward hypotheses on metastasis evolution and therapy in colorectal cancer · 2018
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