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Long Non-coding RNAs in Cancer: Implications for Diagnosis, Prognosis, and Therapy

Yuchen Qian, Lei Shi, Zhong Luo

Frontiers in Medicine · 2020 · Review · CC BY

doi:10.3389/fmed.2020.612393

Abstract

Long non-coding RNAs (lncRNAs) are major components of cellular transcripts that are arising as important players in various biological pathways. They have received extensive attention in recent years, regarded to be involved in both developmental processes and various diseases. Due to their specific expression and functional diversity in a variety of cancers, lncRNAs have promising applications in cancer diagnosis, prognosis and therapy. Studies have shown that lncRNAs with high specificity and accuracy have the potential to become biomarkers in cancers. LncRNAs can be noninvasively extracted from body fluids, tissues and cells, and can be used as independent or auxiliary biomarkers to improve the accuracy of diagnosis or prognosis. Currently, the most well-recognized lncRNA is PCA3, which has been approved for use in the diagnosis of prostate cancer. Moreover, the underlying mechanisms of lncRNAs were explored as therapeutic targets, which have been investigated in clinical trials of several cancers. In this review, we presented a compilation of recent publications, clinical trials and patents, addressing the potential of lncRNAs that could be considered as biomarkers or therapeutic targets, with the hopes of providing promised implications for future cancer therapy.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 20, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

Cancer is a life-threating disease with rising morbidity and mortality. Despite tremendous progress made in recent years, there are still a number of issues in cancer treatment that need improvements, such as delayed diagnosis and poor prognosis. Most tumor biomarkers or therapeutic targets currently in clinical use are proteins. However, only 2% of human genome is translated into proteins. Therefore, we may need to focus more on non-coding regions, where more cancer mutations occur than in coding regions. In recent years, long non-coding RNAs (lncRNAs), which occupy the majority of non-coding RNAs (ncRNAs), are hotspots in cancer research. Due to the large number of lncRNAs, with an estimate of 102,000, lncRNA-based research holds great promise in cancer treatment.

LncRNAs are non-coding transcripts with more than 200 nucleotides in length, and most of them remain in the nucleus after transcription. Due to their low expression levels, lncRNAs were initially considered to be transcription noise. With better understanding, lncRNAs are found to be involved in transcriptional and post-transcriptional regulation, through interactions with DNA, RNA or proteins. LncRNAs promote or inhibit the formation of transcription loops, and recruit or block regulators, regulating gene transcription. Besides, lncRNAs also regulate mRNA splicing and act as precursors to other ncRNAs, such as microRNAs (miRNAs). LncRNAs function as oncogenes or tumor suppressors, taking part in various signaling pathways. Of note, by analyzing the expression of lncRNAs in peripheral blood, urine sediments or tissue samples, a series of lncRNAs were identified with great promise as auxiliary or independent biomarkers in cancer diagnosis and prognosis.

There are currently few biomarkers or therapeutic agents targeting lncRNAs. Prostate cancer antigen 3 (PCA3), an early diagnostic biomarker for prostate cancer (PCa), is the first and only approved lncRNA for clinical use at this time. There are also some lncRNAs undergoing clinical trials or having been patented, which we will discuss in more details below. Moreover, other research of lncRNA-based drug discoveries, including UBE3A-ATS in Angelman syndrome, SCN1ANAT in Dravet syndrome and SMN-AS1 in spinal muscular atrophy, also illustrate the potential of lncRNAs.

In this review, we discuss the mechanisms by which lncRNAs function. A thorough understanding of these mechanisms is critical for the development of anti-tumor drugs. We next summarize a collection of recent publications, clinical trials, and patents and also discuss the potential of lncRNAs that could be considered as biomarkers or therapeutic targets in cancer diagnosis, prognosis and treatment.

Mechanisms of LncRNAs

Understanding how lncRNAs work is critical to know how they cause diseases such as cancers, and therefore to their potential applications in cancer treatment. Based on current studies, lncRNAs are implicated in many intracellular molecular interaction networks. The levels of their expression are regulated by many factors, and they are also involved in complex networks as regulatory factors. The myriad mechanisms behind these complex regulations can be summarized in four ways, including signal, scaffold, decoy, and guide (Figure 1).

Some lncRNAs are expressed at different levels in various cell states. Thus, they can be turned into signals, serving as indicators to reflect development or disease status. For example, Xist, which is typically transcribed by the inactive X chromosome, can be used to indicate X chromosome inactivation.

LncRNAs can bind proteins and act as scaffolds to assist in the assembly of regulatory complexes. In this way, HOTAIR interacts with polycomb repressive complex 2 (PRC2) to recruit EZH2 to promote H3K27 trimethylation or LSD1 to demethylate H3K4me2.

As decoys, lncRNAs regulate gene expression by preventing the binding of transcription regulators. For example, p53-dependent PANDA inhibits proptosis by directly sequestering of NF-YA. In addition, as competing endogenous RNAs (ceRNAs), lncRNAs also bind miRNAs and prevent RNA degradation. This is common in cancers. H19 acts as ceRNAs both for miR-17-5P in thyroid cancer and for miR-152 in breast cancer.

LncRNAs can also guide the transcription factors to specific sites. In this way, MEG3 guides PRC2 and forms a complex with DNA. It is noteworthy that each type is not mutually exclusive, and an individual lncRNA may have one or more of these functions.

LncRNAs in Cancer Diagnosis

Some lncRNAs are highly tissue specific and abnormally expressed in cancer, which can be extracted noninvasively from the circulation. These features render them potential candidates for cancer diagnosis (Table 1). The one most well-recognized is PCA3, a biomarker for early diagnosis of prostate cancer (PCa). As mentioned above, it has been approved in clinical use. The diagnosis of PCa currently relies on the elevation of serum prostate-specific antigen (PSA). However, its specificity in discriminating benign and malignant tumors is low, which may lead to over-diagnosis in low-risk patients. PSA is a good predictor when its level is above 10 ng/ml. However, in the gray area of PSA, some auxiliary indicators are still needed to improve diagnostic accuracy.

Urine PCA3 diagnosis is not only highly sensitive (58–82%) but also has excellent specificity (59–76%). PCA3 is up-regulated 60 to 100-folds in more than 95% of PCa specimens. It is noteworthy that PCA3-based assays are still effective when cancer cells make up <10% of the examined sample. PCA3 silence leads to an increase in the expression of E-cadherin, Claudin-3, and Keratin-18, while a decrease of Vimentin. The association between PCA3 and these traditional protein biomarkers provides more support for its application as diagnostic marker.

MALAT1 can be used as an auxiliary biomarker to improve the accuracy of early diagnosis, especially in the gray area of PSA. Its diagnostic accuracy is higher than the previous index, free/total PSA ratio. In fact, one of the MALAT1 assay has been patented in PCa diagnosis (CN104498495).

H19 is another lncRNA with high diagnostic sensitivity and specificity. In breast cancer, patient plasma H19 levels were elevated, with an sensitivity of 0.81 (AUC, area under the curve), higher than traditional diagnostic biomarkers. H19 is related to many important miRNAs in the network of cancer-related functions. It is a precursor of miR-675 which has downstream targets like c-CbI, CbI-b and Igf1r. H19/miR-675 also causes the activation of EGRF and c-Met, which leads to the sustained activation of Akt and Erk. Besides, H19 acts as a ceRNA for Let-7 to maintain the activation of breast cancer stem cells. The potential of miRNAs like miR-675 and Let-7 as biomarkers has been reported in cancers, which implicate the diagnostic potential of H19. In gastric cancer (GC), H19 had a high diagnostic ability with an AUC of 0.838. A patent has been filed for gastric cancer diagnosis with HOTAIR and MALAT1 (CN105586399A), showing possible applications. Notably, single nucleotide polymorphisms (SNPs) of H19 are used to predict the risk of cancer, such as rs2839698 and rs2107425 genotypes are found to be related to decreased risk of bladder cancer.

LncRNAs are usually aberrantly expressed and can be extracted noninvasively from the circulation. Although some lncRNAs overlap in various cancer, ~60% of these abnormally expressed lncRNAs are cancer type-specific. Recently, the diagnostic potential of some lncRNAs has been implicated by clinical trials. One report have shown that UCA1 was sensitive for bladder cancer, especially in patients with superficial G2-G3. Another clinical trial is underway to explore the possible application of CCAT1 in CRC (NCT04269746). Moreover, lncRNAs can not only be used as an independent biomarkers, but also can be combined with other lncRNAs or proteins to improve the sensitivity and accuracy of diagnosis.

LncRNAs in Cancer Prognosis

The expression of lncRNAs in cancer correlates with overall survival (OS), metastasis, tumor stage or grade, thus can potentially serve as markers for prognosis (Table 1).

HOTAIR is transcribed from HOXC locus located at 12q13.13. It has been proved to be poor prognostic indicators of various cancers. Bladder transitional cell carcinoma (TCC) patients with high HOTAIR have lower overall survival, and positively associated with histological grade.

An analysis of a large cohort containing 300 samples showed that the increased expression level of HOTAIR in GC tissues was correlated with peritoneal diffusion. In addition, in diffuse GC, tissues with a high HOTAIR level showed more venous infiltration and poorer overall survival. Besides, HOTAIR is involved in tumorigenicity in pancreatic cancer and can also cause CRC proliferation and metastasis mediated by PCR2 complex.

MALAT1, located on chromosome 11q13.1, is dysregulated in many cancers. A cohort analysis of 169 patients showed that patients with high MALAT1 expression levels had a worse prognosis than the normal group. Moreover, upregulated MALAT1 is closely related to hepatocellular carcinoma (HCC) progression, and can be an independent biomarker for recurrence after liver transplantation. However, the roles of MALAT1 in breast cancer are still controversial. In previous reports, MALAT1 acts as a ceRNA for miR-1/CDC42 axis to enhance cell migration and invasion. On the contrary, Kim et al. reported that MALAT1 acted as a metastasis suppressor by preventing the binding of transcription factor TEAD and its co-activator YAP. In addition, MALAT1 knockout leads to different phenotypes in various cell lines and models, and there is no clear explanation for this variation. Therefore, further investigation is required before MALAT1 could be use as a potential prognositic biomarker.

CCAT2 showed extensive effects during proliferation and metastasis in a variety of cancers. In fact, patients with high CCAT2 had a lower overall survival and almost twice the risk of death.

LncRNAs in Cancer Therapy

The aberrant expression of lncRNAs and their involvement in diverse cellular processes make them possible targets for cancer therapy. Clinical studies have demonstrated the importance of studying the mechanisms of lncRNA. BC-819, a plasmid containing the promoter of H19 and coding sequence of diphtheria toxin, has been applied in clinical trials of bladder, pancreatic and ovarian cancer. The H19 promoter allows diphtheria toxin to be specifically expressed in tumor tissues. Thus, BC-819 can effectively ablate tumors, reduce tumor growth, prolong recurrence time, and has low local toxicity. We can also learn about the prospect of lncRNAs from patent applications. For example, an inhibitor of LINC01212 is used to treat melanoma (US2016271163). What's more, lncMyoD, acts directly as functional element on IMP1 and IMP2 for sarcoma therapy (WO2015020960). Furthermore, although lncRNAs are considered with no protein-coding ability, some special lncRNAs can be translated into micropeptides. In fact, some patents utilized these polypeptides for antibodie design in cancer diagnosis and treatment, such as lncRNA-6585 and its antibody in cervical cancers (CN109337903A).

LncRNAs and their loci can be targeted for the design and synthesis of specific nucleic acid sequences in therapy, such as CRISPR/Cas9 design, small interfering RNA (siRNA) and antisense oligonucleotides (ASOs). However, unlike mRNA, most lncRNAs are located in the nucleus and have high-level structure. Oligonucleotide drugs must enter cells and bind to their target RNA to function, which raises challenges for drug delivery and intrinsic affinity. To address these issues, a common approach is to modify the sequence of oligonucleotides, and the development of nanomedicine to improve drug delivery.

CRISPR/Cas9 silencing of NEAT1 or MALAT1 was reported to inhibit metastasis of cancer cells. A patent used CRISPR/Cas9 to silence UCA1 inhibited the growth of cancer cells (CN106399306B). However, due to the overlap of loci, CRISPR/Cas9 cannot be applied to the silencing of all lncRNAs. In a genome-wide study including 15,929 lncRNA loci, only 38% were successfully silenced as expected, while the remaining had a severe negative impact on the expression of neighboring genes.

Both of siRNA and ASOs can effectively and specifically silence the expression of target genes, making them essential tools for research and clinical uses. Despite some challenges, the progress of siRNAs as therapy drugs has evolved from pre-design to clinical trials. Recently, a siRNA targeting DDX11-AS1 has been patented in liver cancer (CN108546702A). Compare to siRNA, ASOs enter the nucleus more efficiently and bind to precursor RNAs near the intron and exon junction, affecting the alternative splicing process.

Methods for affinity and delivery improvement: Affinity of oligonucleotides can be improved by constructing aptamers. They can also be modified to reduce nuclease degradation and increase their internal affinity. For delivery, one effective approach is to construct drug carriers, such as in the form of gold nanoparticles.

Discussion

In recent years, many studies have been devoted to lncRNAs in cancer progression and treatment. Due to their highly specific expression and diverse functions, lncRNAs hold great promise for cancer diagnosis, prognosis and therapy. To the best of our knowledge, however, the sole lncRNA that has been approved in clinical use is PCA3 in the diagnosis of PCa. Although multiple lncRNAs have been extensively investigated in clinical trials or have been patented, their applications still have a long way to go. Here we review potential lncRNAs that could be considered as biomarkers or therapeutic targets and discuss some of the issues that deserve special consideration.

First, the actual mechanisms by which lncRNA act are not fully understood. Indeed, the developing of oligonucleotide drug Genasense can be served as an informative case. Due to the lack of in-depth understanding of the mechanism, the development of Genasense failed, revealing the importance of understanding the mechanism in drug development. Second, the low conservation of lncRNAs, some of which are expressed only in primates, makes it difficult to establish universal experimental models. For the majority of lncRNAs, we have yet to establish a suitable animal model, which is essential for understanding the functions better. Third, although some experiments have been conducted on the applications of lncRNAs, they are not very reliable due to the small sample size. Moreover, for therapeutic targets, it is important to study whether the dysregulated expression of lncRNAs is the cause or a result of cancer.

Although there are many challenges, the prospects and clinical significance of lncRNAs cannot be overlooked in the long run. A distinctive feature of lncRNAs is their high specificity in tumor tissues and cells, making it possible for them to be specific and accurate biomarkers. In addition, abnormally expressed lncRNAs can be extracted non-invasively, showing great potential to be more economical and less harmful. Compared to protein-based anti-tumor drugs, lncRNA are more refined and less toxic, and the low expression of lncRNA means that only a small amount of inhibitors are needed to make a difference. Besides, bioinformatics and computational tools provide new opportunities for lncRNA biomarker development. However, due to the lack of experimental evidence and no further clinical validation, we do not discuss it here. Although there are currently no lncRNA-based oncology drugs, drugs targeting lncRNAs in other diseases will provide useful clinical insights.

In conclusion, the intensive study of lncRNAs has brought new hope for the diagnosis and treatment of cancer. Although limitations exist, such as mechanisms, conservative, and animal models, the successful application of PCA3 is a great source of inspiration and impetus for clinical research on lncRNAs. A comprehensive understanding of lncRNA's expression, structure, and mechanisms will help to open up a new intervention, identifying novel and sensitive biomarkers and therapeutic targets.

Author Contributions

YQ and LS participated in the design of the study, prepared table, figure, and wrote the manuscript. LS and ZL conceived the study and wrote the manuscript. All authors contributed to the article and approved the submitted version.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References 100

  1. 1.

    Bray F Ferlay J Soerjomataram I Siegel RL Torre LA Jemal A Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. (2018 ) 68:394–424.

    Not in our library10.3322/caac.21492

  2. 2.

    Chandra Gupta S Nandan Tripathi Y Potential of long non-coding RNAs in cancer patients, from biomarkers to therapeutic targets. Int J Cancer. (2017 ) 140:1955–67.

    Not in our library10.1002/ijc.30546

  3. 3.

    Cuykendall TN Rubin MA Khurana E Non-coding genetic variation in cancer. Curr Opin Syst Biol. (2017 ) 1:9–15.

    Not in our library10.1016/j.coisb.2016.12.017

  4. 4.

    Zhao Y Li H Fang S Kang Y Wu W Hao Y. NONCODE 2016: an informative and valuable data source of long non-coding RNAs. Nucleic Acids Res. (2016 ) 44:D203–8.

    Not in our library10.1093/nar/gkv1252

  5. 5.

    Wang KC Chang HY Molecular mechanisms of long noncoding RNAs. Mol Cell. (2011 ) 43:904–14.

    Not in our library10.1016/j.molcel.2011.08.018

  6. 6.

    Quinn JJ Chang HY. Unique features of long non-coding RNA biogenesis and function. Nat Rev Genet. (2016 ) 17:47–62.

    Not in our library10.1038/nrg.2015.10

  7. 7.

    Li W Notani D Ma Q Tanasa B Nunez E Chen AY. Functional roles of enhancer RNAs for oestrogen-dependent transcriptional activation. Nature. (2013 ) 498:516–20.

    Not in our library10.1038/nature12210

  8. 8.

    Lai F Orom UA Cesaroni M Beringer M Taatjes DJ Blobel GA. Activating RNAs associate with mediator to enhance chromatin architecture and transcription. Nature. (2013 ) 494:497–501.

    Not in our library10.1038/nature11884

  9. 9.

    Khalil AM Guttman M Huarte M Garber M Raj A Rivea Morales D. Many human large intergenic noncoding RNAs associate with chromatin-modifying complexes and affect gene expression. Proc Natl Acad Sci USA. (2009 ) 106:11667–72.

    Not in our library10.1073/pnas.0904715106

  10. 10.

    Jarroux J Morillon A Pinskaya M. History, discovery, and classification of lncRNAs. Adv Exp Med Biol. (2017 ) 1008:1–46.

    Not in our library10.1007/978-981-10-5203-3_1

  11. 11.

    Huarte M. The emerging role of lncRNAs in cancer. Nat Med. (2015 ) 21:1253–61.

    Not in our library10.1038/nm.3981

  12. 12.

    Smolle MA Bauernhofer T Pummer K Calin GA Pichler M. Current insights into long non-coding RNAs (LncRNAs) in prostate cancer. Int J Mol Sci. (2017 ) 18:473.

    Not in our library10.3390/ijms18020473

  13. 13.

    Groskopf J Aubin SM Deras IL Blase A Bodrug S Clark C. APTIMA PCA3 molecular urine test: development of a method to aid in the diagnosis of prostate cancer. Clin Chem. (2006 ) 52:1089–95.

    Not in our library10.1373/clinchem.2005.063289

  14. 14.

    Meng L Ward AJ Chun S Bennett CF Beaudet AL Rigo F. Towards a therapy for Angelman syndrome by targeting a long non-coding RNA. Nature. (2015 ) 518:409–12.

    Not in our library10.1038/nature13975

  15. 15.

    Hsiao J Yuan TY Tsai MS Lu CY Lin YC Lee ML. Upregulation of haploinsufficient gene expression in the brain by targeting a long non-coding RNA improves seizure phenotype in a model of dravet syndrome. EBioMedicine. (2016 ) 9:257–77.

    Not in our library10.1016/j.ebiom.2016.05.011

  16. 16.

    d'Ydewalle C Ramos DM Pyles NJ Ng SY Gorz M Pilato CM. The antisense transcript SMN-AS1 regulates SMN expression and is a novel therapeutic target for spinal muscular atrophy. Neuron. (2017 ) 93:66–79.

    Not in our library10.1016/j.neuron.2016.11.033

  17. 17.

    Woo CJ Maier VK Davey R Brennan J Li G Brothers J. Gene activation of SMN by selective disruption of lncRNA-mediated recruitment of PRC2 for the treatment of spinal muscular atrophy. Proc Natl Acad Sci USA. (2017 ) 114:E1509–18.

    Not in our library10.1073/pnas.1616521114

  18. 18.
    Mechanisms of long noncoding RNA function in development and disease · 2016
    No notice
  19. 19.

    Balas MM Johnson AM. Exploring the mechanisms behind long noncoding RNAs and cancer. Noncoding RNA Res. (2018 ) 3:108–17.

    Not in our library10.1016/j.ncrna.2018.03.001

  20. 20.

    Kazemzadeh M Safaralizadeh R Orang AV. LncRNAs: emerging players in gene regulation and disease pathogenesis. J Genet. (2015 ) 94:771–84.

    Not in our library10.1007/s12041-015-0561-6

  21. 21.

    Pontier DB Gribnau J. Xist regulation and function explored. Hum Genet. (2011 ) 130:223–36.

    Not in our library10.1007/s00439-011-1008-7

  22. 22.
    The Implication of Early Chromatin Changes in X Chromosome Inactivation · 2019
    No notice
  23. 23.

    Zappulla DC Cech TR. Yeast telomerase RNA: a flexible scaffold for protein subunits. Proc Natl Acad Sci USA. (2004 ) 101:10024–9.

    Not in our library10.1073/pnas.0403641101

  24. 24.

    Rinn JL Kertesz M Wang JK Squazzo SL Xu X Brugmann SA. Functional demarcation of active and silent chromatin domains in human HOX loci by noncoding RNAs. Cell. (2007 ) 129:1311–23.

    Not in our library10.1016/j.cell.2007.05.022

  25. 25.

    Rinn JL Chang HY. Genome regulation by long noncoding RNAs. Annu Rev Biochem. (2012 ) 81:145–66.

    Not in our library10.1146/annurev-biochem-051410-092902

  26. 26.
    Long noncoding RNA PANDA and scaffold-attachment-factor SAFA control senescence entry and exit · 2014
    No notice
  27. 27.

    Li Z Li Y Li Y Ren K Li X Han X. Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152. J Biochem Mol Toxicol. (2017 ) 31:e21933.

    Not in our library10.1002/jbt.21933

  28. 28.

    Liu L Yang J Zhu X Li D Lv Z Zhang X. Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer. FEBS J. (2016 ) 283:2326–39.

    Not in our library10.1111/febs.13741

  29. 29.

    Hung T Chang HY. Long noncoding RNA in genome regulation: prospects and mechanisms. RNA Biol. (2010 ) 7:582–5.

    Not in our library10.4161/rna.7.5.13216

  30. 30.
    MEG3 long noncoding RNA regulates the TGF-β pathway genes through formation of RNA–DNA triplex structures · 2015
    Corrected
  31. 31.

    Yan X Hu Z Feng Y Hu X Yuan J Zhao SD. Comprehensive genomic characterization of long non-coding RNAs across human cancers. Cancer Cell. (2015 ) 28:529–40.

    Not in our library10.1016/j.ccell.2015.09.006

  32. 32.

    Schmitt AM Chang HY. Long noncoding RNAs in cancer pathways. Cancer Cell. (2016 ) 29:452–63.

    Not in our library10.1016/j.ccell.2016.03.010

  33. 33.

    Hessels D Klein Gunnewiek JM van Oort I Karthaus HF van Leenders GJ van Balken B. DD3(PCA3)-based molecular urine analysis for the diagnosis of prostate cancer. Eur Urol. (2003 ) 44:8–15. discussion: 15–6.

    Not in our library10.1016/s0302-2838(03)00201-x

  34. 34.

    Lemos AE Ferreira LB Batoreu NM de Freitas PP Bonamino MH Gimba ER. PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells. Tumour Biol. (2016 ) 37:11339–48.

    Not in our library10.1007/s13277-016-5012-3

  35. 35.

    Salameh A Lee AK Cardo-Vila M Nunes DN Efstathiou E Staquicini FI. PRUNE2 is a human prostate cancer suppressor regulated by the intronic long noncoding RNA PCA3. Proc Natl Acad Sci USA. (2015 ) 112:8403–8.

    Not in our library10.1073/pnas.1507882112

  36. 36.

    Ren S Wang F Shen J Sun Y Xu W Lu J. Long non-coding RNA metastasis associated in lung adenocarcinoma transcript 1 derived miniRNA as a novel plasma-based biomarker for diagnosing prostate cancer. Eur J Cancer. (2013 ) 49:2949–59.

    Not in our library10.1016/j.ejca.2013.04.026

  37. 37.
    LncRNA-p21 alters the antiandrogen enzalutamide-induced prostate cancer neuroendocrine differentiation via modulating the EZH2/STAT3 signaling · 2019
    No notice
  38. 38.
    Exosome–transmitted long non-coding RNA PTENP1 suppresses bladder cancer progression · 2018
    No notice
  39. 39.

    Xue M Pang H Li X Li H Pan J Chen W. Long non-coding RNA urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN1 pathway. Cancer Sci. (2016 ) 107:18–27.

    Not in our library10.1111/cas.12844

  40. 40.

    Liu D Li Y Luo G Xiao X Tao D Wu X. LncRNA SPRY4-IT1 sponges miR-101-3p to promote proliferation and metastasis of bladder cancer cells through up-regulating EZH2. Cancer Lett. (2017 ) 388:281–91.

    Not in our library10.1016/j.canlet.2016.12.005

  41. 41.

    Sun X Du P Yuan W Du Z Yu M Yu X. Long non-coding RNA HOTAIR regulates cyclin J via inhibition of microRNA-205 expression in bladder cancer. Cell Death Dis. (2015 ) 6:e1907.

    Not in our library10.1038/cddis.2015.269

  42. 42.

    Zhang K Luo Z Zhang Y Zhang L Wu L Liu L. Circulating lncRNA H19 in plasma as a novel biomarker for breast cancer. Cancer Biomark. (2016 ) 17:187–94.

    Not in our library10.3233/cbm-160630

  43. 43.

    Zhan H Tu S Zhang F Shao A Lin J. MicroRNAs and long non-coding RNAs in c-Met-regulated cancers. Front Cell Dev Biol. (2020 ) 8:145.

    Not in our library10.3389/fcell.2020.00145

  44. 44.

    Chou J Wang B Zheng T Li X Zheng L Hu J. MALAT1 induced migration and invasion of human breast cancer cells by competitively binding miR-1 with cdc42. Biochem Biophys Res Commun. (2016 ) 472:262–9.

    Not in our library10.1016/j.bbrc.2016.02.102

  45. 45.

    Kim J Piao HL Kim BJ Yao F Han Z Wang Y. Long noncoding RNA MALAT1 suppresses breast cancer metastasis. Nat Genet. (2018 ) 50:1705–15.

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

  46. 46.

    Younger ST L J. Rinn: 'Lnc'-ing enhancers to MYC regulation. Cell Res. (2014 ) 24:643–4.

    Not in our library10.1038/cr.2014.54

  47. 47.

    Ling H Spizzo R Atlasi Y Nicoloso M Shimizu M Redis RS. CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer. Genome Res. (2013 ) 23:1446–61.

    Not in our library10.1101/gr.152942.112

  48. 48.

    Zhang X Xu Y He C Guo X Zhang J He C. Elevated expression of CCAT2 is associated with poor prognosis in esophageal squamous cell carcinoma. J Surg Oncol. (2015 ) 111:834–9.

    Not in our library10.1002/jso.23888

  49. 49.

    Xu C Yang M Tian J Wang X Li Z. MALAT-1: a long non-coding RNA and its important 3' end functional motif in colorectal cancer metastasis. Int J Oncol. (2011 ) 39:169–75.

    Not in our library10.3892/ijo.2011.1007

  50. 50.

    Zhang X Zhou Y Mehta KR Danila DC Scolavino S Johnson SR. A pituitary-derived MEG3 isoform functions as a growth suppressor in tumor cells. J Clin Endocrinol Metab. (2003 ) 88:5119–26.

    Not in our library10.1210/jc.2003-030222

  51. 51.

    Kogo R Shimamura T Mimori K Kawahara K Imoto S Sudo T. Long noncoding RNA HOTAIR regulates polycomb-dependent chromatin modification and is associated with poor prognosis in colorectal cancers. Cancer Res. (2011 ) 71:6320–6.

    Not in our library10.1158/0008-5472.can-11-1021

  52. 52.

    Kim K Jutooru I Chadalapaka G Johnson G Frank J Burghardt R. HOTAIR is a negative prognostic factor and exhibits pro-oncogenic activity in pancreatic cancer. Oncogene. (2013 ) 32:1616–25.

    Not in our library10.1038/onc.2012.193

  53. 53.

    Zhang J Qiu WQ Zhu H Liu H Sun JH Chen Y. HOTAIR contributes to the carcinogenesis of gastric cancer via modulating cellular and exosomal miRNAs level. Cell Death Dis. (2020 ) 11:780.

    Not in our library10.1038/s41419-020-02946-4

  54. 54.

    Elsayed ET Salem PE Darwish AM Fayed HM. Plasma long non-coding RNA HOTAIR as a potential biomarker for gastric cancer. Int J Biol Markers. (2018 ) 33:1724600818760244.

    Not in our library10.1177/1724600818760244

  55. 55.

    Okugawa Y Toiyama Y Hur K Toden S Saigusa S Tanaka K. Metastasis-associated long non-coding RNA drives gastric cancer development and promotes peritoneal metastasis. Carcinogenesis. (2014 ) 35:2731–9.

    Not in our library10.1093/carcin/bgu200

  56. 56.
    Enhanced Expression of Long Non-Coding RNA HOTAIR Is Associated with the Development of Gastric Cancer · 2013
    No notice
  57. 57.

    Sun W Yang Y Xu C Xie Y Guo J. Roles of long noncoding RNAs in gastric cancer and their clinical applications. J Cancer Res Clin Oncol. (2016 ) 142:2231–7.

    Not in our library10.1007/s00432-016-2183-7

  58. 58.

    Li L Geng Y Feng R Zhu Q Miao B Cao J. The human RNA surveillance factor UPF1 modulates gastric cancer progression by targeting long non-coding RNA MALAT1. Cell Physiol Biochem. (2017 ) 42:2194–206.

    Not in our library10.1159/000479994

  59. 59.

    Xia H Chen Q Chen Y Ge X Leng W Tang Q. The lncRNA MALAT1 is a novel biomarker for gastric cancer metastasis. Oncotarget. (2016 ) 7:56209–18.

    Not in our library10.18632/oncotarget.10941

  60. 60.
    lncRNA involvement in hepatocellular carcinoma metastasis and prognosis · 2018
    No notice
  61. 61.

    Liu D Zhu Y Pang J Weng X Feng X Guo Y. Knockdown of long non-coding RNA MALAT1 inhibits growth and motility of human hepatoma cells via modulation of miR-195. J Cell Biochem. (2018 ) 119:1368–80.

    Not in our library10.1002/jcb.26297

  62. 62.

    Li C Miao R Liu S Wan Y Zhang S Deng Y. Down-regulation of miR-146b-5p by long noncoding RNA MALAT1 in hepatocellular carcinoma promotes cancer growth and metastasis. Oncotarget. (2017 ) 8:28683–95.

    Not in our library10.18632/oncotarget.15640

  63. 63.

    Shi WH Wu QQ Li SQ Yang TX Liu ZH Tong YS. Upregulation of the long noncoding RNA PCAT-1 correlates with advanced clinical stage and poor prognosis in esophageal squamous carcinoma. Tumour Biol. (2015 ) 36:2501–7.

    Not in our library10.1007/s13277-014-2863-3

  64. 64.

    Wang P Liu YH Yao YL Li Z Li ZQ Ma J. Long non-coding RNA CASC2 suppresses malignancy in human gliomas by miR-21. Cell Signal. (2015 ) 27:275–82.

    Not in our library10.1016/j.cellsig.2014.11.011

  65. 65.

    Wang Y Wang Y Li J Zhang Y Yin H Han B. CRNDE, a long-noncoding RNA, promotes glioma cell growth and invasion through mTOR signaling. Cancer Lett. (2015 ) 367:122–8.

    Not in our library10.1016/j.canlet.2015.03.027

  66. 66.

    Di W Li Q Shen W Guo H Zhao S. The long non-coding RNA HOTAIR promotes thyroid cancer cell growth, invasion and migration through the miR-1-CCND2 axis. Am J Cancer Res. (2017 ) 7:1298–1309.

    Not in our library

  67. 67.

    Xu YH Deng JL Wang G Zhu YS. Long non-coding RNAs in prostate cancer: functional roles and clinical implications. Cancer Lett. (2019 ) 464:37–55.

    Not in our library10.1016/j.canlet.2019.08.010

  68. 68.

    Leyten GH Hessels D Jannink SA Smit FP de Jong H Cornel EB. Prospective multicentre evaluation of PCA3 and TMPRSS2-ERG gene fusions as diagnostic and prognostic urinary biomarkers for prostate cancer. Eur Urol. (2014 ) 65:534–42.

    Not in our library10.1016/j.eururo.2012.11.014

  69. 69.
    Development and prospective multicenter evaluation of the long noncoding RNA MALAT-1 as a diagnostic urinary biomarker for prostate cancer · 2014
    No notice
  70. 70.

    Ghafouri-Fard S Esmaeili M Taheri M. H19 lncRNA: roles in tumorigenesis. Biomed Pharmacother. (2020 ) 123:109774.

    Not in our library10.1016/j.biopha.2019.109774

  71. 71.
    H19 non coding RNA-derived miR-675 enhances tumorigenesis and metastasis of breast cancer cells by downregulating c-Cbl and Cbl-b · 2015
    No notice
  72. 72.

    Keniry A Oxley D Monnier P Kyba M Dandolo L Smits G. The H19 lincRNA is a developmental reservoir of miR-675 that suppresses growth and Igf1r. Nat Cell Biol. (2012 ) 14:659–65.

    Not in our library10.1038/ncb2521

  73. 73.
    H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance · 2017
    Corrected
  74. 74.
    Let ‐ 7 as biomarker, prognostic indicator, and therapy for precision medicine in cancer · 2019
    No notice
  75. 75.

    Verhaegh GW Verkleij L Vermeulen SH den Heijer M Witjes JA Kiemeney LA. Polymorphisms in the H19 gene and the risk of bladder cancer. Eur Urol. (2008 ) 54:1118–26.

    Not in our library10.1016/j.eururo.2008.01.060

  76. 76.

    Yu X Li Z Zheng H Chan MT Wu WK. NEAT1: a novel cancer-related long non-coding RNA. Cell Prolif. (2017 ) 50:e12329.

    Not in our library10.1111/cpr.12329

  77. 77.

    Wang XS Zhang Z Wang HC Cai JL Xu QW Li MQ. Rapid identification of UCA1 as a very sensitive and specific unique marker for human bladder carcinoma. Clin Cancer Res. (2006 ) 12:4851–8.

    Not in our library10.1158/1078-0432.ccr-06-0134

  78. 78.
    HOTAIR: an oncogenic long non-coding RNA in different cancers. · 2015
    No notice
  79. 79.

    Zheng HT Shi DB Wang YW Li XX Xu Y Tripathi P. High expression of lncRNA MALAT1 suggests a biomarker of poor prognosis in colorectal cancer. Int J Clin Exp Pathol. (2014 ) 7:3174–81.

    Not in our library

  80. 80.

    Lai MC Yang Z Zhou L Zhu QQ Xie HY Zhang F. Long non-coding RNA MALAT-1 overexpression predicts tumor recurrence of hepatocellular carcinoma after liver transplantation. Med Oncol. (2012 ) 29:1810–6.

    Not in our library10.1007/s12032-011-0004-z

  81. 81.

    Arun G Spector DL. MALAT1 long non-coding RNA and breast cancer. RNA Biol. (2019 ) 16:860–3.

    Not in our library10.1080/15476286.2019.1592072

  82. 82.

    Gutschner T Hammerle M Diederichs S. MALAT1 – a paradigm for long noncoding RNA function in cancer. J Mol Med. (2013 ) 91:791–801.

    Not in our library10.1007/s00109-013-1028-y

  83. 83.

    Smaldone MC Davies BJ. BC-819, a plasmid comprising the H19 gene regulatory sequences and diphtheria toxin A, for the potential targeted therapy of cancers. Curr Opin Mol Ther. (2010 ) 12:607–16.

    Not in our library

  84. 84.

    Hanna N Ohana P Konikoff FM Leichtmann G Hubert A Appelbaum L. Phase 1/2a, dose-escalation, safety, pharmacokinetic and preliminary efficacy study of intratumoral administration of BC-819 in patients with unresectable pancreatic cancer. Cancer Gene Ther. (2012 ) 19:374–81.

    Not in our library10.1038/cgt.2012.10

  85. 85.

    Gofrit ON Benjamin S Halachmi S Leibovitch I Dotan Z Lamm DL. DNA based therapy with diphtheria toxin-A BC-819: a phase 2b marker lesion trial in patients with intermediate risk nonmuscle invasive bladder cancer. J Urol. (2014 ) 191:1697–702.

    Not in our library10.1016/j.juro.2013.12.011

  86. 86.

    Zhang Y Tang L. The application of lncRNAs in cancer treatment and diagnosis. Recent Pat Anticancer Drug Discov. (2018 ) 13:292–301.

    Not in our library10.2174/1574892813666180226121819

  87. 87.

    Anderson DM Anderson KM Chang CL Makarewich CA Nelson BR McAnally JR. A micropeptide encoded by a putative long noncoding RNA regulates muscle performance. Cell. (2015 ) 160:595–606.

    Not in our library10.1016/j.cell.2015.01.009

  88. 88.
    Cellular localization of long non-coding RNAs affects silencing by RNAi more than by antisense oligonucleotides · 2015
    No notice
  89. 89.
    Localization and abundance analysis of human lncRNAs at single-cell and single-molecule resolution · 2015
    No notice
  90. 90.

    Bennett CF Swayze EE. RNA targeting therapeutics: molecular mechanisms of antisense oligonucleotides as a therapeutic platform. Annu Rev Pharmacol Toxicol. (2010 ) 50:259–93.

    Not in our library10.1146/annurev.pharmtox.010909.105654

  91. 91.

    Goyal A Myacheva K Gross M Klingenberg M Duran Arque B Diederichs S. Challenges of CRISPR/Cas9 applications for long non-coding RNA genes. Nucleic Acids Res. (2017 ) 45:e12.

    Not in our library10.1093/nar/gkw883

  92. 92.

    Ozcan G Ozpolat B Coleman RL Sood AK Lopez-Berestein G. Preclinical and clinical development of siRNA-based therapeutics. Adv Drug Deliv Rev. (2015 ) 87:108–9.

    Not in our library10.1016/j.addr.2015.01.007

  93. 93.

    Matsui M Corey DR. Non-coding RNAs as drug targets. Nat Rev Drug Discov. (2017 ) 16:167–79.

    Not in our library10.1038/nrd.2016.117

  94. 94.

    Renganathan A Felley-Bosco E. Long noncoding RNAs in cancer and therapeutic potential. Adv Exp Med Biol. (2017 ) 1008:199–222.

    Not in our library10.1007/978-981-10-5203-3_7

  95. 95.

    Nulf CJ Corey D. Intracellular inhibition of hepatitis C virus (HCV) internal ribosomal entry site (IRES)-dependent translation by peptide nucleic acids (PNAs) and locked nucleic acids (LNAs). Nucleic Acids Res. (2004 ) 32:3792–8.

    Not in our library10.1093/nar/gkh706

  96. 96.

    Nielsen PE Egholm M Berg RH Buchardt O. Sequence-selective recognition of DNA by strand displacement with a thymine-substituted polyamide. Science. (1991 ) 254:1497–500.

    Not in our library10.1126/science.1962210

  97. 97.

    Gong N Teng X Li J Liang XJ. Antisense oligonucleotide-conjugated nanostructure-targeting lncRNA MALAT1 inhibits cancer metastasis. ACS Appl Mater Interfaces. (2019 ) 11:37–42.

    Not in our library10.1021/acsami.8b18288

  98. 98.

    Boon RA Jae N Holdt L Dimmeler S. Long noncoding RNAs: from clinical genetics to therapeutic targets? J Am Coll Cardiol. (2016 ) 67:1214–26.

    Not in our library10.1016/j.jacc.2015.12.051

  99. 99.

    Bhan A Soleimani M Mandal SS. Long noncoding RNA and cancer: a new paradigm. Cancer Res. (2017 ) 77:3965–81.

    Not in our library10.1158/0008-5472.can-16-2634

  100. 100.

    Huang R Zhou L Chi Y Wu H Shi L. LncRNA profile study reveals a seven-lncRNA signature predicts the prognosis of patients with colorectal cancer. Biomark Res. (2020 ) 8:8.

    Not in our library10.1186/s40364-020-00187-3

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