For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
13
views
92
references
 Top references
cited by
18
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      641
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The role of m6A methylation in therapy resistance in cancer

      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

          Cancer therapy resistance is the main cause of cancer treatment failure. The mechanism of therapy resistance is a hot topic in epigenetics. As one of the most common RNA modifications, N6-methyladenosine (m6A) is involved in various processes of RNA metabolism, such as stability, splicing, transcription, translation, and degradation. A large number of studies have shown that m6A RNA methylation regulates the proliferation and invasion of cancer cells, but the role of m6A in cancer therapy resistance is unclear. In this review, we summarized the research progress related to the role of m6A in regulating therapy resistance in cancers.

          Related collections

          Most cited references92

          • Record: found
          • Abstract: found
          • Article: not found
          Is Open Access

          Cancer statistics, 2022

          Rebecca Siegel, Kimberly D Miller, Hannah Fuchs … (2022)
          Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths in the United States and compiles the most recent data on population-based cancer occurrence and outcomes. Incidence data (through 2018) were collected by the Surveillance, Epidemiology, and End Results program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data (through 2019) were collected by the National Center for Health Statistics. In 2022, 1,918,030 new cancer cases and 609,360 cancer deaths are projected to occur in the United States, including approximately 350 deaths per day from lung cancer, the leading cause of cancer death. Incidence during 2014 through 2018 continued a slow increase for female breast cancer (by 0.5% annually) and remained stable for prostate cancer, despite a 4% to 6% annual increase for advanced disease since 2011. Consequently, the proportion of prostate cancer diagnosed at a distant stage increased from 3.9% to 8.2% over the past decade. In contrast, lung cancer incidence continued to decline steeply for advanced disease while rates for localized-stage increased suddenly by 4.5% annually, contributing to gains both in the proportion of localized-stage diagnoses (from 17% in 2004 to 28% in 2018) and 3-year relative survival (from 21% to 31%). Mortality patterns reflect incidence trends, with declines accelerating for lung cancer, slowing for breast cancer, and stabilizing for prostate cancer. In summary, progress has stagnated for breast and prostate cancers but strengthened for lung cancer, coinciding with changes in medical practice related to cancer screening and/or treatment. More targeted cancer control interventions and investment in improved early detection and treatment would facilitate reductions in cancer mortality.
          Article 0 comments Cited 5798 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Primary, Adaptive, and Acquired Resistance to Cancer Immunotherapy.

            Padmanee Sharma, Siwen Hu-Lieskovan, Jennifer A. Wargo … (2017)
            Cancer immunotherapy can induce long lasting responses in patients with metastatic cancers of a wide range of histologies. Broadening the clinical applicability of these treatments requires an improved understanding of the mechanisms limiting cancer immunotherapy. The interactions between the immune system and cancer cells are continuous, dynamic, and evolving from the initial establishment of a cancer cell to the development of metastatic disease, which is dependent on immune evasion. As the molecular mechanisms of resistance to immunotherapy are elucidated, actionable strategies to prevent or treat them may be derived to improve clinical outcomes for patients.
            Article 0 comments Cited 1604 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 1220 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Jian Wang: 1627879372@qq.com
                Yang Jiao: jiaoyang@suda.edu.cn
                Lili Wang: wanglili@suda.edu.cn
                Journal
                Journal ID (nlm-ta): Mol Cancer
                Journal ID (iso-abbrev): Mol Cancer
                Title: Molecular Cancer
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1476-4598
                Publication date (Electronic): 1 June 2023
                Publication date PMC-release: 1 June 2023
                Publication date Collection: 2023
                Volume: 22
                Electronic Location Identifier: 91
                Affiliations
                [1 ]GRID grid.429222.d, ISNI 0000 0004 1798 0228, Department of Radiation Oncology, , The First Affiliated Hospital of Soochow University, ; Suzhou, 21500 China
                [2 ]Department of Radiotherapy, The Affiliated Jiangyin People’s Hospital of Nantong University, Jiangyin, 214400 China
                [3 ]GRID grid.263761.7, ISNI 0000 0001 0198 0694, Department of Radiation Oncology, , Dushu Lake Hospital Affiliated to Soochow University, ; Suzhou, 21500 China
                [4 ]GRID grid.263761.7, ISNI 0000 0001 0198 0694, School of Radiation Medicine and Protection, , Medical College of Soochow University, ; Suzhou, 215000 China
                Article
                Publisher ID: 1782
                DOI: 10.1186/s12943-023-01782-2
                PMC ID: 10233906
                PubMed ID: 37264402
                SO-VID: 4b0607b3-b527-4173-a9ff-16573c79c9b0
                Copyright © © The Author(s) 2023
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

                History
                Date received : 24 February 2023
                Date accepted : 24 April 2023
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © BioMed Central Ltd., part of Springer Nature 2023

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: m6a methylation,cancer,chemoresistance,radiotherapy resistance
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: m6a methylation, cancer, chemoresistance, radiotherapy resistance

                Comments

                Comment on this article

                scite_

                Similar content641

                See all similar

                Cited by18

                See all cited by

                Most referenced authors1,480

                See all reference authors