For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
9
views
150
references
 Top references
cited by
31
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      98
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The role of M 6A modification in the regulation of tumor-related lncRNAs

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          N 6-methyladenosine (m 6A) is the most abundant modification in eukaryotic cells, and it regulates RNA transcription, processing, splicing, degradation, and translation. Long non-coding RNAs (lncRNAs), as transcriptional products with no or limited protein coding ability more than 200 nt in length, play an important role in epigenetic modification, mRNA transcription, splicing, stability, translation, and other biological functions. Extensive studies have shown that both m 6A modification and lncRNAs are involved in the pathogenesis of various diseases, such as kinds of cancers, heart failure, Alzheimer’s disease, periodontitis, human abdominal aortic aneurysm, and obesity. To date, m 6A modification has been identified as an important biological function in enrichment and regulation of lncRNAs. In this review, we summarize the role of m 6A modification in the regulation and function of tumor-related lncRNAs. Moreover, we discuss the potential applications and possible future directions in the field.

          Graphical abstract

          Abstract

          In this review, we summarize the role of m 6A modification in the regulation and function of tumor-related lncRNAs. Moreover, we discuss the potential applications and possible future directions in the field.

          Related collections

          Most cited references150

          • Record: found
          • Abstract: found
          • Article: not found

          Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq.

          Dan Dominissini, Sharon Moshitch-Moshkovitz, Schraga Schwartz … (2012)
          An extensive repertoire of modifications is known to underlie the versatile coding, structural and catalytic functions of RNA, but it remains largely uncharted territory. Although biochemical studies indicate that N(6)-methyladenosine (m(6)A) is the most prevalent internal modification in messenger RNA, an in-depth study of its distribution and functions has been impeded by a lack of robust analytical methods. Here we present the human and mouse m(6)A modification landscape in a transcriptome-wide manner, using a novel approach, m(6)A-seq, based on antibody-mediated capture and massively parallel sequencing. We identify over 12,000 m(6)A sites characterized by a typical consensus in the transcripts of more than 7,000 human genes. Sites preferentially appear in two distinct landmarks--around stop codons and within long internal exons--and are highly conserved between human and mouse. Although most sites are well preserved across normal and cancerous tissues and in response to various stimuli, a subset of stimulus-dependent, dynamically modulated sites is identified. Silencing the m(6)A methyltransferase significantly affects gene expression and alternative splicing patterns, resulting in modulation of the p53 (also known as TP53) signalling pathway and apoptosis. Our findings therefore suggest that RNA decoration by m(6)A has a fundamental role in regulation of gene expression.
          Article 0 comments Cited 1365 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Comprehensive analysis of mRNA methylation reveals enrichment in 3' UTRs and near stop codons.

            Kate D Meyer, Yogesh Saletore, Paul Zumbo … (2012)
            Methylation of the N(6) position of adenosine (m(6)A) is a posttranscriptional modification of RNA with poorly understood prevalence and physiological relevance. The recent discovery that FTO, an obesity risk gene, encodes an m(6)A demethylase implicates m(6)A as an important regulator of physiological processes. Here, we present a method for transcriptome-wide m(6)A localization, which combines m(6)A-specific methylated RNA immunoprecipitation with next-generation sequencing (MeRIP-Seq). We use this method to identify mRNAs of 7,676 mammalian genes that contain m(6)A, indicating that m(6)A is a common base modification of mRNA. The m(6)A modification exhibits tissue-specific regulation and is markedly increased throughout brain development. We find that m(6)A sites are enriched near stop codons and in 3' UTRs, and we uncover an association between m(6)A residues and microRNA-binding sites within 3' UTRs. These findings provide a resource for identifying transcripts that are substrates for adenosine methylation and reveal insights into the epigenetic regulation of the mammalian transcriptome. Copyright © 2012 Elsevier Inc. All rights reserved.
            Article 0 comments Cited 1175 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              N6-Methyladenosine in Nuclear RNA is a Major Substrate of the Obesity-Associated FTO

              Guifang Jia, Ye Fu, Xu Zhao … (2011)
              We report here that FTO (fat mass and obesity-associated protein) exhibits efficient oxidative demethylation activity of abundant N 6-methyladenosine (m6A) residues in RNA in vitro. FTO knockdown with siRNA led to an increased level of m6A in mRNA, whereas overexpression of FTO resulted in a decreased level of m6A in human cells. We further show that FTO partially colocalizes with nuclear speckles, supporting m6A in nuclear RNA as a physiological substrate of FTO.
              Article 0 comments Cited 1093 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Hongbo Guo
                Journal
                Journal ID (nlm-ta): Mol Ther Nucleic Acids
                Journal ID (iso-abbrev): Mol Ther Nucleic Acids
                Title: Molecular Therapy. Nucleic Acids
                Publisher: American Society of Gene & Cell Therapy
                ISSN (Electronic): 2162-2531
                Publication date PMC-release: 09 April 2021
                Publication date Collection: 04 June 2021
                Publication date (Electronic): 09 April 2021
                Volume: 24
                Pages: 768-779
                Affiliations
                [1 ]Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China
                Author notes
                [∗ ]Corresponding author: Hongbo Guo, Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China. guohongbo911@ 123456126.com
                [2]

                These authors contributed equally

                Article
                Publisher Item ID: S2162-2531(21)00096-2
                DOI: 10.1016/j.omtn.2021.04.002
                PMC ID: 8094576
                PubMed ID: 33996258
                SO-VID: 5f072c4d-80b9-4c9c-8003-57d64af86f7c
                Copyright © © 2021 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: lncrna,n6-methyladenosine,methylation modification,tumor,biological function
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: lncrna, n6-methyladenosine, methylation modification, tumor, biological function

                Comments

                Comment on this article

                scite_

                Similar content98

                See all similar

                Cited by31

                See all cited by

                Most referenced authors2,664

                See all reference authors