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• W3047950076 abstract "N6-methyladenosine (m6A) is the most common RNA modification and has an important role in normal development and tumorigenesis. The abnormal expression of m6A regulators can lead to an imbalance in m6A levels in cancer cells, leading to the dysregulated expression of oncogenes and tumor suppressor genes that may contribute to cancer development, patient response to chemoradiotherapy, and clinical prognosis. Recent studies demonstrate that non-coding RNAs are involved in epigenetic modification of both DNA and RNA in tumor cells, and may also affect the development and progression of cancer by targeting m6A regulators. In this review, we describe the functional crosstalk between m6A and non-coding RNAs, particularly microRNA, long non-coding RNA, and circular RNA, and illustrate their roles in tumor regulation. Finally, we discuss the significance of non-coding RNA and m6A modification in the diagnosis, treatment, and prognosis of cancer patients, as well as potential future research directions. N6-methyladenosine (m6A) is the most common RNA modification and has an important role in normal development and tumorigenesis. The abnormal expression of m6A regulators can lead to an imbalance in m6A levels in cancer cells, leading to the dysregulated expression of oncogenes and tumor suppressor genes that may contribute to cancer development, patient response to chemoradiotherapy, and clinical prognosis. Recent studies demonstrate that non-coding RNAs are involved in epigenetic modification of both DNA and RNA in tumor cells, and may also affect the development and progression of cancer by targeting m6A regulators. In this review, we describe the functional crosstalk between m6A and non-coding RNAs, particularly microRNA, long non-coding RNA, and circular RNA, and illustrate their roles in tumor regulation. Finally, we discuss the significance of non-coding RNA and m6A modification in the diagnosis, treatment, and prognosis of cancer patients, as well as potential future research directions. According to recent global cancer statistics, cancer remains an important factor threatening human health.1Siegel R.L. Miller K.D. Jemal A. Cancer statistics, 2020.CA Cancer J. Clin. 2020; 70: 7-30Crossref PubMed Scopus (10742) Google Scholar N6-methyladenosine (m6A) is the most common RNA modification and has attracted significant attention from researchers in the fields of tumorigenesis and development.2Lan Q. Liu P.Y. Haase J. Bell J.L. Hüttelmaier S. Liu T. The Critical Role of RNA m6A Methylation in Cancer.Cancer Res. 2019; 79: 1285-1292Crossref PubMed Scopus (303) Google Scholar,3Dai D. Wang H. Zhu L. Jin H. Wang X. N6-methyladenosine links RNA metabolism to cancer progression.Cell Death Dis. 2018; 9: 124Crossref PubMed Scopus (236) Google Scholar Since the discovery of m6A in the early 1970s, studies have shown that it accumulates predominantly near the stop codons and 3′ untranslated regions (3′ UTRs) of mRNA.4Meyer K.D. Saletore Y. Zumbo P. Elemento O. Mason C.E. Jaffrey S.R. Comprehensive analysis of mRNA methylation reveals enrichment in 3′ UTRs and near stop codons.Cell. 2012; 149: 1635-1646Abstract Full Text Full Text PDF PubMed Scopus (2079) Google Scholar, 5Alarcón C.R. Lee H. Goodarzi H. Halberg N. Tavazoie S.F. N6-methyladenosine marks primary microRNAs for processing.Nature. 2015; 519: 482-485Crossref PubMed Scopus (687) Google Scholar, 6Zhao B.S. Roundtree I.A. He C. Post-transcriptional gene regulation by mRNA modifications.Nat. Rev. Mol. Cell Biol. 2017; 18: 31-42Crossref PubMed Scopus (917) Google Scholar, 7Lee M. Kim B. Kim V.N. Emerging roles of RNA modification: m(6)A and U-tail.Cell. 2014; 158: 980-987Abstract Full Text Full Text PDF PubMed Scopus (178) Google Scholar, 8Desrosiers R. Friderici K. Rottman F. Identification of methylated nucleosides in messenger RNA from Novikoff hepatoma cells.Proc. Natl. Acad. Sci. USA. 1974; 71: 3971-3975Crossref PubMed Scopus (889) Google Scholar The abnormal expression of m6A regulators can lead to an imbalance in m6A levels in cancer cells, leading to the dysregulated expression of oncogenes and tumor suppressor genes that may contribute to cancer development, patient response to chemoradiotherapy, and clinical prognosis.2Lan Q. Liu P.Y. Haase J. Bell J.L. Hüttelmaier S. Liu T. The Critical Role of RNA m6A Methylation in Cancer.Cancer Res. 2019; 79: 1285-1292Crossref PubMed Scopus (303) Google Scholar,7Lee M. Kim B. Kim V.N. Emerging roles of RNA modification: m(6)A and U-tail.Cell. 2014; 158: 980-987Abstract Full Text Full Text PDF PubMed Scopus (178) Google Scholar,9Deng X. Su R. Weng H. Huang H. Li Z. Chen J. RNA N6-methyladenosine modification in cancers: current status and perspectives.Cell Res. 2018; 28: 507-517Crossref PubMed Scopus (318) Google Scholar,10Du J. Hou K. Mi S. Ji H. Ma S. Ba Y. Hu S. Xie R. Chen L. Malignant Evaluation and Clinical Prognostic Values of m6A RNA Methylation Regulators in Glioblastoma.Front. Oncol. 2020; 10: 208Crossref PubMed Scopus (23) Google Scholar Previous studies confirm that dysregulation of m6A regulators may be detected in precancerous lesions, highlighting their potential as molecular markers for the early diagnosis of cancer.11Huang W. Qi C.B. Lv S.W. Xie M. Feng Y.Q. Huang W.H. Yuan B.F. Determination of DNA and RNA Methylation in Circulating Tumor Cells by Mass Spectrometry.Anal. Chem. 2016; 88: 1378-1384Crossref PubMed Scopus (91) Google Scholar Fat mass and obesity-associated protein (FTO) has been identified as an m6A demethylase that can selectively remove the m6A modification from target RNAs.12Jia G. Fu Y. Zhao X. Dai Q. Zheng G. Yang Y. Yi C. Lindahl T. Pan T. Yang Y.G. He C. N6-methyladenosine in nuclear RNA is a major substrate of the obesity-associated FTO.Nat. Chem. Biol. 2011; 7: 885-887Crossref PubMed Scopus (1952) Google Scholar A recent study showed that combination of FTO inhibitor and nilotinib can restrain the growth of leukemia and increase the sensitivity of leukemia cells to tyrosine kinase inhibitors, highlighting the potential therapeutic value of targeting m6A regulators in drug-resistant cancers.13Yan F. Al-Kali A. Zhang Z. Liu J. Pang J. Zhao N. He C. Litzow M.R. Liu S. A dynamic N6-methyladenosine methylome regulates intrinsic and acquired resistance to tyrosine kinase inhibitors.Cell Res. 2018; 28: 1062-1076Crossref PubMed Scopus (86) Google Scholar Although the FTO inhibitor, entacapone, has been approved by The Food and Drug Administration (FDA) for the treatment of cancer and other related diseases,14Major J.M. Dong D. Cunningham F. By K. Hur K. Shih D.C. Jiang R. Podskalny G.D. Wei X. Pinheiro S. et al.Entacapone and prostate cancer in Parkinson’s disease patients: A large Veterans Affairs healthcare system study.Parkinsonism Relat. Disord. 2018; 53: 46-52Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar specific inhibitors have not yet been identified for other m6A regulatory proteins. Although the function of m6A modification in cancer is becoming increasingly clear, its effect on protein translation and the molecular mechanisms underlying the effect of this mark on cancer progression remain unclear. Following the development of MeRIP-seq (methylated RNA immunoprecipitation sequencing) and miCLIP (m6A individual-nucleotide-resolution cross-linking and immunoprecipitation) technologies, researchers have found that non-coding RNAs, including long non-coding RNA (lncRNA), microRNA (miRNA), circular RNA (circRNA), transfer RNA, ribosomal RNA, and small nuclear RNA, are also capable of modifying DNA and RNA bases in cancer cells.15Pendleton K.E. Chen B. Liu K. Hunter O.V. Xie Y. Tu B.P. Conrad N.K. The U6 snRNA m6A Methyltransferase METTL16 Regulates SAM Synthetase Intron Retention.Cell. 2017; 169: 824-835.e14Abstract Full Text Full Text PDF PubMed Scopus (443) Google Scholar,16Du Y. Hou G. Zhang H. Dou J. He J. Guo Y. Li L. Chen R. Wang Y. Deng R. et al.SUMOylation of the m6A-RNA methyltransferase METTL3 modulates its function.Nucleic Acids Res. 2018; 46: 5195-5208Crossref PubMed Scopus (125) Google Scholar Furthermore, non-coding RNA also participates in the regulation of m6A modification, thus affecting cancer progression (Figure 1).3Dai D. Wang H. Zhu L. Jin H. Wang X. N6-methyladenosine links RNA metabolism to cancer progression.Cell Death Dis. 2018; 9: 124Crossref PubMed Scopus (236) Google Scholar,17Fazi F. Fatica A. Interplay Between N6-Methyladenosine (m6A) and Non-coding RNAs in Cell Development and Cancer.Front. Cell Dev. Biol. 2019; 7: 116Crossref PubMed Scopus (70) Google Scholar In this review, we describe the functional crosstalk between m6A and non-coding RNA, particularly miRNA, lncRNA, and circRNA, and illustrate how deregulation of these networks plays a role in tumors. Finally, we discuss the significance of non-coding RNA and m6A modifications in the diagnosis, treatment, and prognosis of cancer patients and possible future research directions. m6A modification is a dynamic and reversible process that has a critical role in regulating RNA stability, splicing, and translation. This modification is controlled by regulatory proteins referred to as “writers,” “erasers,” and “readers” (Figure 2). Epigenetic writers included methyltransferase-like 3/14/16 (METTL3/14/16), wt1-associated protein (WTAP), RNA binding motif protein 15/15B (RBM15/15B), and vir-like m6A methyltransferase-associated protein (VIRMA, also known as KIAA1429). METTL3/14 can form complexes to cause m6A methylation to be written into mRNA,18Cui Q. Shi H. Ye P. Li L. Qu Q. Sun G. Sun G. Lu Z. Huang Y. Yang C.G. et al.m6A RNA Methylation Regulates the Self-Renewal and Tumorigenesis of Glioblastoma Stem Cells.Cell Rep. 2017; 18: 2622-2634Abstract Full Text Full Text PDF PubMed Scopus (654) Google Scholar and WTAP aids METTL3/14 to locate nuclear spots and maintain the catalytic activity of m6A methyltransferase in vivo.19Ping X.L. Sun B.F. Wang L. Xiao W. Yang X. Wang W.J. Adhikari S. Shi Y. Lv Y. Chen Y.S. et al.Mammalian WTAP is a regulatory subunit of the RNA N6-methyladenosine methyltransferase.Cell Res. 2014; 24: 177-189Crossref PubMed Scopus (1095) Google Scholar Meanwhile, METTL3 expression is essential for WTAP protein homeostasis.20Sorci M. Ianniello Z. Cruciani S. Larivera S. Ginistrelli L.C. Capuano E. Marchioni M. Fazi F. Fatica A. METTL3 regulates WTAP protein homeostasis.Cell Death Dis. 2018; 9: 796Crossref PubMed Scopus (69) Google Scholar Moreover, RBM15, RBM15B, and VIRMA have roles in the regulation of METTL3 and METTL14 activity.21Ianniello Z. Fatica A. N6-Methyladenosine Role in Acute Myeloid Leukaemia.Int. J. Mol. Sci. 2018; 19: 2345Crossref PubMed Scopus (32) Google Scholar Erasers include FTO and AlkB homolog 5 (ALKBH5). These proteins can selectively remove the m6A mark targeting mRNA through a series of complex intermediate reactions, thereby affecting tumor-specific biological processes.22Huang Y. Yan J. Li Q. Li J. Gong S. Zhou H. Gan J. Jiang H. Jia G.F. Luo C. Yang C.G. Meclofenamic acid selectively inhibits FTO demethylation of m6A over ALKBH5.Nucleic Acids Res. 2015; 43: 373-384Crossref PubMed Scopus (294) Google Scholar In 2001, researchers from the laboratory of Chuan He confirmed that FTO is an important DNA and RNA demethylase, particularly for m6A demethylation.12Jia G. Fu Y. Zhao X. Dai Q. Zheng G. Yang Y. Yi C. Lindahl T. Pan T. Yang Y.G. He C. N6-methyladenosine in nuclear RNA is a major substrate of the obesity-associated FTO.Nat. Chem. Biol. 2011; 7: 885-887Crossref PubMed Scopus (1952) Google Scholar The oncogenic role of FTO has since been confirmed in numerous cancers, including cervical cancer, breast cancer (BRC), and gastric cancer (GC).23Zou D. Dong L. Li C. Yin Z. Rao S. Zhou Q. The m6A eraser FTO facilitates proliferation and migration of human cervical cancer cells.Cancer Cell Int. 2019; 19: 321Crossref PubMed Scopus (69) Google Scholar, 24Niu Y. Lin Z. Wan A. Chen H. Liang H. Sun L. Wang Y. Li X. Xiong X.F. Wei B. et al.RNA N6-methyladenosine demethylase FTO promotes breast tumor progression through inhibiting BNIP3.Mol. Cancer. 2019; 18: 46Crossref PubMed Scopus (247) Google Scholar, 25Ge L. Zhang N. Chen Z. Song J. Wu Y. Li Z. Chen F. Wu J. Li D. Li J. et al.Level of N6-Methyladenosine in Peripheral Blood RNA: A Novel Predictive Biomarker for Gastric Cancer.Clin. Chem. 2020; 66: 342-351Crossref PubMed Scopus (26) Google Scholar To date, several hypotheses have inferred that m6A modifications function by altering RNA structure or recruiting m6A readers. The most common readers include m6A RNA binding protein 1/2/3 (YTHDF1/2/3), YTH domain-containing 1/2 (YTHDC1/2), insulin-like growth factor 2 mRNA binding proteins 1/2/3 (IGF2BP1/2/3), heterogeneous nuclear ribonucleoproteins (HNRNPs), and zinc-finger CCCH domain-containing protein 13 (ZC3H13).26Meyer K.D. Jaffrey S.R. Rethinking m6A Readers, Writers, and Erasers.Annu. Rev. Cell Dev. Biol. 2017; 33: 319-342Crossref PubMed Scopus (488) Google Scholar Reader proteins function by binding to m6A sites on the target RNA and mediating its modification, thereby controlling RNA fate.26Meyer K.D. Jaffrey S.R. Rethinking m6A Readers, Writers, and Erasers.Annu. Rev. Cell Dev. Biol. 2017; 33: 319-342Crossref PubMed Scopus (488) Google Scholar,27Chen M. Wong C.M. The emerging roles of N6-methyladenosine (m6A) deregulation in liver carcinogenesis.Mol. Cancer. 2020; 19: 44Crossref PubMed Scopus (101) Google Scholar In addition to revealing the functional roles and mechanisms of m6A RNA methylation in various cancers, recent studies highlighted the impact of m6A RNA methylation regulators on the diagnosis and prognosis of cancer patients (Table 1). Du et al.10Du J. Hou K. Mi S. Ji H. Ma S. Ba Y. Hu S. Xie R. Chen L. Malignant Evaluation and Clinical Prognostic Values of m6A RNA Methylation Regulators in Glioblastoma.Front. Oncol. 2020; 10: 208Crossref PubMed Scopus (23) Google Scholar performed univariate Cox regression analysis to evaluate the clinical prognostic values of m6A RNA methylation regulators in glioblastoma (GBM), and revealed that HNRNPC, ALKBH5, and ZC3H13 are favorable prognostic markers, whereas FTO is an unfavorable prognostic marker for GBM. Furthermore, METTL3, YTHDC2, and YTHDF2 were identified as independent predictors of overall survival in liver cancer (LC).28Wang W. Sun B. Xia Y. Sun S. He C. RNA N6-Methyladenosine-Related Gene Contribute to Clinical Prognostic Impact on Patients With Liver Cancer.Front. Genet. 2020; 11: 306Crossref PubMed Scopus (7) Google Scholar Moreover, Zhuang et al.29Zhuang Z. Chen L. Mao Y. Zheng Q. Li H. Huang Y. Hu Z. Jin Y. Diagnostic, progressive and prognostic performance of m6A methylation RNA regulators in lung adenocarcinoma.Int. J. Biol. Sci. 2020; 16: 1785-1797Crossref PubMed Scopus (30) Google Scholar built a 10-gene risk score model in lung adenocarcinoma (LUAD) through combined analysis of expression levels of m6A RNA regulators and clinicopathological characters. They found that the expression patterns of ALKBH5, FTO, HNRNPC, YTHDF2, YTHDF1, YTHDC2, RBM15, KIAA1429, WTAP, and METTL3 were correlated with TNM stage, lymph node stage, and sex, as well as the living status of patients with LUAD. A two-gene signature consisting of METTL3 and METTL14 was identified as an independent prognostic indicator for distinguishing clear cell renal cell carcinoma (ccRCC) patients.30Chen J. Yu K. Zhong G. Shen W. Identification of a m6A RNA methylation regulators-based signature for predicting the prognosis of clear cell renal carcinoma.Cancer Cell Int. 2020; 20: 157Crossref PubMed Scopus (24) Google Scholar These studies suggested that m6A regulators are potential diagnostic and prognostic markers for various cancers.Table 1Impact of m6A Modification Regulator on Diagnosis and Prognosis of Cancer PatientsCancer Typem6A RegulatorDiagnosis/PrognosisReferencesGBMHNRNPC, ZC3H13, ALKBH5unfavorable prognostic marker10Du J. Hou K. Mi S. Ji H. Ma S. Ba Y. Hu S. Xie R. Chen L. Malignant Evaluation and Clinical Prognostic Values of m6A RNA Methylation Regulators in Glioblastoma.Front. Oncol. 2020; 10: 208Crossref PubMed Scopus (23) Google ScholarFTOfavorable prognostic markerLCMETTL3, YTHDC2, YTHDF2unfavorable prognostic marker28Wang W. Sun B. Xia Y. Sun S. He C. RNA N6-Methyladenosine-Related Gene Contribute to Clinical Prognostic Impact on Patients With Liver Cancer.Front. Genet. 2020; 11: 306Crossref PubMed Scopus (7) Google ScholarLUADALKBH5, HNRNPC, YTHDF2, YTHDF1, YTHDC2, RBM15, KIAA1429, WTAP, METTL3, FTOdiagnostic marker, prognostic marker29Zhuang Z. Chen L. Mao Y. Zheng Q. Li H. Huang Y. Hu Z. Jin Y. Diagnostic, progressive and prognostic performance of m6A methylation RNA regulators in lung adenocarcinoma.Int. J. Biol. Sci. 2020; 16: 1785-1797Crossref PubMed Scopus (30) Google ScholarccRCCMETTL3unfavorable prognostic marker30Chen J. Yu K. Zhong G. Shen W. Identification of a m6A RNA methylation regulators-based signature for predicting the prognosis of clear cell renal carcinoma.Cancer Cell Int. 2020; 20: 157Crossref PubMed Scopus (24) Google ScholarMETTL14favorable prognostic marker Open table in a new tab Non-coding RNAs comprise a large class of RNA transcripts without protein-coding potential that regulate gene expression and are important regulators of cancer cell proliferation, apoptosis, migration, immune response, and autophagy.31Beermann J. Piccoli M.T. Viereck J. Thum T. Non-coding RNAs in Development and Disease: Background, Mechanisms, and Therapeutic Approaches.Physiol. Rev. 2016; 96: 1297-1325Crossref PubMed Scopus (991) Google Scholar m6A modification of non-coding RNA regulates important processes controlling RNA function, including processing, stability, and transport (Figure 3).32Huang H. Weng H. Chen J. m6A Modification in Coding and Non-coding RNAs: Roles and Therapeutic Implications in Cancer.Cancer Cell. 2020; 37: 270-288Abstract Full Text Full Text PDF PubMed Scopus (290) Google Scholar On the basis of our current understanding, miRNA biogenesis can be divided into three steps.33Rupaimoole R. Slack F.J. MicroRNA therapeutics: towards a new era for the management of cancer and other diseases.Nat. Rev. Drug Discov. 2017; 16: 203-222Crossref PubMed Scopus (2554) Google Scholar In the nucleus, RNA polymerase II or III transcribes miRNA-related genes into primary miRNA (pri-miRNA). pri-miRNA is transformed into precursor miRNA (pre-miRNA) by the microprocessor complex, DGCR8-Drosha, and is subsequently transported out of the nucleus by the exportin-5-Ran-GTP complex. Finally, the microprocessor component, Dicer, cleaves the pre-miRNA into mature mRNA in the cytoplasm.34Bartel D.P. MicroRNAs: genomics, biogenesis, mechanism, and function.Cell. 2004; 116: 281-297Abstract Full Text Full Text PDF PubMed Scopus (28561) Google Scholar,35Mirihana Arachchilage G. Dassanayake A.C. Basu S. A potassium ion-dependent RNA structural switch regulates human pre-miRNA 92b maturation.Chem. Biol. 2015; 22: 262-272Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar miRNAs have important roles in the regulation of gene expression, mainly through their association with AGO2 as part of the RNA-induced silencing complex (RISC), via binding to mRNA 3′ UTR, leading to degradation and inhibition of translation.36Bartel D.P. MicroRNAs: target recognition and regulatory functions.Cell. 2009; 136: 215-233Abstract Full Text Full Text PDF PubMed Scopus (15317) Google Scholar,37Fabian M.R. Sonenberg N. Filipowicz W. Regulation of mRNA translation and stability by microRNAs.Annu. Rev. Biochem. 2010; 79: 351-379Crossref PubMed Scopus (2175) Google Scholar In 2002, the Croce team first identified the role of miRNAs in cancer, demonstrating low expression of miR-15 and miR-16 in chronic lymphocytic leukemia patients.38Calin G.A. Dumitru C.D. Shimizu M. Bichi R. Zupo S. Noch E. Aldler H. Rattan S. Keating M. Rai K. et al.Frequent deletions and down-regulation of micro- RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia.Proc. Natl. Acad. Sci. USA. 2002; 99: 15524-15529Crossref PubMed Scopus (4105) Google Scholar Since then, numerous studies have indicated that abnormal expression of miRNA underlies many pathological processes related to tumorigenesis.39Ha M. Kim V.N. Regulation of microRNA biogenesis.Nat. Rev. Mol. Cell Biol. 2014; 15: 509-524Crossref PubMed Scopus (3290) Google Scholar Notably, there is a strong association between m6A and miRNA binding sites in mammals.4Meyer K.D. Saletore Y. Zumbo P. Elemento O. Mason C.E. Jaffrey S.R. Comprehensive analysis of mRNA methylation reveals enrichment in 3′ UTRs and near stop codons.Cell. 2012; 149: 1635-1646Abstract Full Text Full Text PDF PubMed Scopus (2079) Google Scholar The synthesis and function of miRNAs may be affected by m6A modification at multiple levels (Table 2). Studies by Alarcón et al.40Alarcón C.R. Goodarzi H. Lee H. Liu X. Tavazoie S. Tavazoie S.F. HNRNPA2B1 Is a Mediator of m(6)A-Dependent Nuclear RNA Processing Events.Cell. 2015; 162: 1299-1308Abstract Full Text Full Text PDF PubMed Scopus (667) Google Scholar indicate that heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) can read m6A marks and enhance DGCR8 binding to pri-miRNA transcripts, affecting miRNA processing. Similarly, the m6A writer METTL14 can interact with DGCR8 and promote miR-126 processing in an m6A-dependent manner in hepatocellular carcinoma (HCC).41Ma J.Z. Yang F. Zhou C.C. Liu F. Yuan J.H. Wang F. Wang T.T. Xu Q.G. Zhou W.P. Sun S.H. METTL14 suppresses the metastatic potential of hepatocellular carcinoma by modulating N6 -methyladenosine-dependent primary MicroRNA processing.Hepatology. 2017; 65: 529-543Crossref PubMed Scopus (464) Google Scholar In bladder cancer, METTL3 is overexpressed and regulates the processing of miR-221/miR-222 in an m6A-dependent manner via recruitment of DCGR8.42Han J. Wang J.Z. Yang X. Yu H. Zhou R. Lu H.C. Yuan W.B. Lu J.C. Zhou Z.J. Lu Q. et al.METTL3 promote tumor proliferation of bladder cancer by accelerating pri-miR221/222 maturation in m6A-dependent manner.Mol. Cancer. 2019; 18: 110Crossref PubMed Scopus (258) Google Scholar METTL3 also promotes pri-miR-1246 maturation via a similar mechanism and positively modulates tumor cell metastasis.43Peng W. Li J. Chen R. Gu Q. Yang P. Qian W. Ji D. Wang Q. Zhang Z. Tang J. Sun Y. Upregulated METTL3 promotes metastasis of colorectal Cancer via miR-1246/SPRED2/MAPK signaling pathway.J. Exp. Clin. Cancer Res. 2019; 38: 393Crossref PubMed Scopus (145) Google Scholar Studies by Zhang et al.44Zhang J. Bai R. Li M. Ye H. Wu C. Wang C. Li S. Tan L. Mai D. Li G. et al.Excessive miR-25-3p maturation via N6-methyladenosine stimulated by cigarette smoke promotes pancreatic cancer progression.Nat. Commun. 2019; 10: 1858Crossref PubMed Scopus (146) Google Scholar emphasize the importance of the m6A writer METTL3 on miR-25-3p maturation and identified NKAP as an m6A reader for pri-miR-25 processing in pancreatic cancer (PAC). METTL3 can accelerate the brain metastasis of cancer cells and promote the splicing of pre-miR-143-3p to produce mature miRNA, and may be associated with Dicer in lung cancer (LCA).45Wang H. Deng Q. Lv Z. Ling Y. Hou X. Chen Z. Dinglin X. Ma S. Li D. Wu Y. et al.N6-methyladenosine induced miR-143-3p promotes the brain metastasis of lung cancer via regulation of VASH1.Mol. Cancer. 2019; 18: 181Crossref PubMed Scopus (103) Google Scholar As previously discussed, m6A promotes miRNA maturation by regulating its processing, thereby enhancing the degradation and translational inhibition of downstream target mRNAs.Table 2m6A Modification Regulates miRNA Processingm6A RegulatorAssociated CancerFunctionReferencesReaderHNRNPA2B1BRCpromotes miRNAs processing40Alarcón C.R. Goodarzi H. Lee H. Liu X. Tavazoie S. Tavazoie S.F. HNRNPA2B1 Is a Mediator of m(6)A-Dependent Nuclear RNA Processing Events.Cell. 2015; 162: 1299-1308Abstract Full Text Full Text PDF PubMed Scopus (667) Google ScholarWriterMETTL14HCCpromotes the processing of miR-126 via DGCR841Ma J.Z. Yang F. Zhou C.C. Liu F. Yuan J.H. Wang F. Wang T.T. Xu Q.G. Zhou W.P. Sun S.H. METTL14 suppresses the metastatic potential of hepatocellular carcinoma by modulating N6 -methyladenosine-dependent primary MicroRNA processing.Hepatology. 2017; 65: 529-543Crossref PubMed Scopus (464) Google ScholarMETTL3BLCpromotes the processing of miR-221/222 via DGCR842Han J. Wang J.Z. Yang X. Yu H. Zhou R. Lu H.C. Yuan W.B. Lu J.C. Zhou Z.J. Lu Q. et al.METTL3 promote tumor proliferation of bladder cancer by accelerating pri-miR221/222 maturation in m6A-dependent manner.Mol. Cancer. 2019; 18: 110Crossref PubMed Scopus (258) Google ScholarMETTL3CRCpromotes the processing of miR-1246 by DGCR843Peng W. Li J. Chen R. Gu Q. Yang P. Qian W. Ji D. Wang Q. Zhang Z. Tang J. Sun Y. Upregulated METTL3 promotes metastasis of colorectal Cancer via miR-1246/SPRED2/MAPK signaling pathway.J. Exp. Clin. Cancer Res. 2019; 38: 393Crossref PubMed Scopus (145) Google ScholarMETTL3PACpromotes miR-25-3p maturation44Zhang J. Bai R. Li M. Ye H. Wu C. Wang C. Li S. Tan L. Mai D. Li G. et al.Excessive miR-25-3p maturation via N6-methyladenosine stimulated by cigarette smoke promotes pancreatic cancer progression.Nat. Commun. 2019; 10: 1858Crossref PubMed Scopus (146) Google ScholarMETTL3LCApromotes splicing of pre-miR-143-3p45Wang H. Deng Q. Lv Z. Ling Y. Hou X. Chen Z. Dinglin X. Ma S. Li D. Wu Y. et al.N6-methyladenosine induced miR-143-3p promotes the brain metastasis of lung cancer via regulation of VASH1.Mol. Cancer. 2019; 18: 181Crossref PubMed Scopus (103) Google Scholar Open table in a new tab Interestingly, m6A modifications can also protect mRNA degradation mediated by miRNA. Müller et al.46Müller S. Glaß M. Singh A.K. Haase J. Bley N. Fuchs T. Lederer M. Dahl A. Huang H. Chen J. et al.IGF2BP1 promotes SRF-dependent transcription in cancer in a m6A- and miRNA-dependent manner.Nucleic Acids Res. 2019; 47: 375-390Crossref PubMed Scopus (159) Google Scholar demonstrated that IGF2BP1 affects miRNA-directed decay of SRF mRNA, increasing SRF expression in an m6A-dependent manner. In colorectal cancer (CRC), IGF2BP2 maintains RAF1 mRNA stability by blocking miRNA-mediated degradation, thereby increasing cancer cell proliferation.47Ye S. Song W. Xu X. Zhao X. Yang L. IGF2BP2 promotes colorectal cancer cell proliferation and survival through interfering with RAF-1 degradation by miR-195.FEBS Lett. 2016; 590: 1641-1650Crossref PubMed Scopus (51) Google Scholar Furthermore, m6A modification of AGO2 mRNA has also been reported to affect miRNA levels.48Min K.W. Zealy R.W. Davila S. Fomin M. Cummings J.C. Makowsky D. Mcdowell C.H. Thigpen H. Hafner M. Kwon S.H. et al.Profiling of m6A RNA modifications identified an age-associated regulation of AGO2 mRNA stability.Aging Cell. 2018; 17: e12753Crossref PubMed Scopus (54) Google Scholar In conclusion, m6A modification plays an important role in miRNA biogenesis, and the effects of m6A-mediated miRNA level variation require further investigation. The role of lncRNA in tumor development is complex and diverse.49Wang J. Zhang X. Chen W. Hu X. Li J. Liu C. Regulatory roles of long noncoding RNAs implicated in cancer hallmarks.Int. J. Cancer. 2020; 146: 906-916Crossref PubMed Scopus (46) Google Scholar lncRNAs may regulate gene transcription via binding to gene promoters,50Wang X. Sun W. Shen W. Xia M. Chen C. Xiang D. Ning B. Cui X. Li H. Li X. et al.Long non-coding RNA DILC regulates liver cancer stem cells via IL-6/STAT3 axis.J. 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• W3047950076 title "Crosstalk between RNA m6A Modification and Non-coding RNA Contributes to Cancer Growth and Progression" @default.
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