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The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis

The m(6)A RNA methylation is the most prevalent internal modification in mammalian mRNAs which plays critical biological roles by regulating vital cellular processes. Dysregulations of the m(6)A modification due to aberrant expression of its regulatory proteins are frequently observed in many pathol...

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Autores principales: Uddin, Mohammad Burhan, Wang, Zhishan, Yang, Chengfeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019509/
https://www.ncbi.nlm.nih.gov/pubmed/33814008
http://dx.doi.org/10.1186/s12943-021-01356-0
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author Uddin, Mohammad Burhan
Wang, Zhishan
Yang, Chengfeng
author_facet Uddin, Mohammad Burhan
Wang, Zhishan
Yang, Chengfeng
author_sort Uddin, Mohammad Burhan
collection PubMed
description The m(6)A RNA methylation is the most prevalent internal modification in mammalian mRNAs which plays critical biological roles by regulating vital cellular processes. Dysregulations of the m(6)A modification due to aberrant expression of its regulatory proteins are frequently observed in many pathological conditions, particularly in cancer. Normal cells undergo malignant transformation via activation or modulation of different oncogenic signaling pathways through complex mechanisms. Accumulating evidence showing regulation of oncogenic signaling pathways at the epitranscriptomic level has added an extra layer of the complexity. In particular, recent studies demonstrated that, in many types of cancers various oncogenic signaling pathways are modulated by the m(6)A modification in the target mRNAs as well as noncoding RNA transcripts. m(6)A modifications in these RNA molecules control their fate and metabolism by regulating their stability, translation or subcellular localizations. In this review we discussed recent exciting studies on oncogenic signaling pathways that are modulated by the m(6)A RNA modification and/or their regulators in cancer and provided perspectives for further studies. The regulation of oncogenic signaling pathways by the m(6)A modification and its regulators also render them as potential druggable targets for the treatment of cancer.
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spelling pubmed-80195092021-04-05 The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis Uddin, Mohammad Burhan Wang, Zhishan Yang, Chengfeng Mol Cancer Review The m(6)A RNA methylation is the most prevalent internal modification in mammalian mRNAs which plays critical biological roles by regulating vital cellular processes. Dysregulations of the m(6)A modification due to aberrant expression of its regulatory proteins are frequently observed in many pathological conditions, particularly in cancer. Normal cells undergo malignant transformation via activation or modulation of different oncogenic signaling pathways through complex mechanisms. Accumulating evidence showing regulation of oncogenic signaling pathways at the epitranscriptomic level has added an extra layer of the complexity. In particular, recent studies demonstrated that, in many types of cancers various oncogenic signaling pathways are modulated by the m(6)A modification in the target mRNAs as well as noncoding RNA transcripts. m(6)A modifications in these RNA molecules control their fate and metabolism by regulating their stability, translation or subcellular localizations. In this review we discussed recent exciting studies on oncogenic signaling pathways that are modulated by the m(6)A RNA modification and/or their regulators in cancer and provided perspectives for further studies. The regulation of oncogenic signaling pathways by the m(6)A modification and its regulators also render them as potential druggable targets for the treatment of cancer. BioMed Central 2021-04-04 /pmc/articles/PMC8019509/ /pubmed/33814008 http://dx.doi.org/10.1186/s12943-021-01356-0 Text en © The Author(s) 2021 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.
spellingShingle Review
Uddin, Mohammad Burhan
Wang, Zhishan
Yang, Chengfeng
The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis
title The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis
title_full The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis
title_fullStr The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis
title_full_unstemmed The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis
title_short The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis
title_sort m(6)a rna methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019509/
https://www.ncbi.nlm.nih.gov/pubmed/33814008
http://dx.doi.org/10.1186/s12943-021-01356-0
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