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      The role of m 6A RNA methylation in human cancer

      review-article
      , ,
      Molecular Cancer
      BioMed Central
      N6-methyladenosine, Cancer, RNA methylation, Prognosis, Growth, Metastasis

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          Abstract

          N 6-methyladenosine (m 6A) is identified as the most common, abundant and conserved internal transcriptional modification, especially within eukaryotic messenger RNAs (mRNAs). M 6A modification is installed by the m 6A methyltransferases (METTL3/14, WTAP, RBM15/15B and KIAA1429, termed as “writers”), reverted by the demethylases (FTO and ALKBH5, termed as “erasers”) and recognized by m 6A binding proteins (YTHDF1/2/3, IGF2BP1 and HNRNPA2B1, termed as “readers”). Acumulating evidence shows that, m 6A RNA methylation has an outsize effect on RNA production/metabolism and participates in the pathogenesis of multiple diseases including cancers. Until now, the molecular mechanisms underlying m 6A RNA methylation in various tumors have not been comprehensively clarified. In this review, we mainly summarize the recent advances in biological function of m 6A modifications in human cancer and discuss the potential therapeutic strategies.

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          Most cited references31

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          Rethinking m6A Readers, Writers, and Erasers.

          In recent years, m6A has emerged as an abundant and dynamically regulated modification throughout the transcriptome. Recent technological advances have enabled the transcriptome-wide identification of m6A residues, which in turn has provided important insights into the biology and regulation of this pervasive regulatory mark. Also central to our current understanding of m6A are the discovery and characterization of m6A readers, writers, and erasers. Over the last few years, studies into the function of these proteins have led to important discoveries about the regulation and function of m6A. However, during this time our understanding of these proteins has also evolved considerably, sometimes leading to the reversal of early concepts regarding the reading, writing and erasing of m6A. In this review, we summarize recent advances in m6A research, and we highlight how these new findings have reshaped our understanding of how m6A is regulated in the transcriptome.
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            Ythdc2 is an N6-methyladenosine binding protein that regulates mammalian spermatogenesis

            N 6 -methyladenosine (m 6 A) is the most common internal modification in eukaryotic mRNA. It is dynamically installed and removed, and acts as a new layer of mRNA metabolism, regulating biological processes including stem cell pluripotency, cell differentiation, and energy homeostasis. m 6 A is recognized by selective binding proteins; YTHDF1 and YTHDF3 work in concert to affect the translation of m 6 A-containing mRNAs, YTHDF2 expedites mRNA decay, and YTHDC1 affects the nuclear processing of its targets. The biological function of YTHDC2, the final member of the YTH protein family, remains unknown. We report that YTHDC2 selectively binds m 6 A at its consensus motif. YTHDC2 enhances the translation efficiency of its targets and also decreases their mRNA abundance. Ythdc2 knockout mice are infertile; males have significantly smaller testes and females have significantly smaller ovaries compared to those of littermates. The germ cells of Ythdc2 knockout mice do not develop past the zygotene stage and accordingly, Ythdc2 is upregulated in the testes as meiosis begins. Thus, YTHDC2 is an m 6 A-binding protein that plays critical roles during spermatogenesis.
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              N6-methyladenosine (m6A) recruits and repels proteins to regulate mRNA homeostasis

              A comprehensive proteomics screen for ‘reader’ proteins that recognize m6A-modified RNA reveals that the modification both promotes and prevents the binding of factors that control mRNA homeostasis in mammalian cells.
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                Author and article information

                Contributors
                xiaoyu643@163.com
                jing5522724@vip.163.com
                +86-21-24058970 , zhujs1803@163.com
                Journal
                Mol Cancer
                Mol. Cancer
                Molecular Cancer
                BioMed Central (London )
                1476-4598
                29 May 2019
                29 May 2019
                2019
                : 18
                : 103
                Affiliations
                ISNI 0000 0004 1798 5117, GRID grid.412528.8, Department of Gastroenterology, , Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, ; Yishan Road 600, Shanghai, 200233 China
                Author information
                http://orcid.org/0000-0002-8646-0176
                Article
                1033
                10.1186/s12943-019-1033-z
                6540575
                31142332
                2f1d6d58-fdb0-4671-bdb4-7734bb8f711d
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 18 March 2019
                : 22 May 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81873143
                Award ID: 81573747
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100003399, Science and Technology Commission of Shanghai Municipality;
                Award ID: 17411966500
                Award Recipient :
                Categories
                Review
                Custom metadata
                © The Author(s) 2019

                Oncology & Radiotherapy
                n6-methyladenosine,cancer,rna methylation,prognosis,growth,metastasis
                Oncology & Radiotherapy
                n6-methyladenosine, cancer, rna methylation, prognosis, growth, metastasis

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