4.8 Review

Crosstalk between m6A regulators and mRNA during cancer progression

Journal

ONCOGENE
Volume 41, Issue 39, Pages 4407-4419

Publisher

SPRINGERNATURE
DOI: 10.1038/s41388-022-02441-4

Keywords

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Funding

  1. National Natural Science Foundation of China [81902532, 82072773]
  2. China Postdoctoral Science Foundation [2022M712255]
  3. National Key Research and Development Program of China
  4. Stem Cell and Translational Research [2017YFA0106500]
  5. Distinguished Young Scientists Program of Sichuan Province [2019JDJQ0029]
  6. 1.3.5 project for disciplines of excellence, West China Hospital, Sichuan University [ZYYC20019]

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The m(6)A modification, a prevalent and abundant RNA modification, is involved in the occurrence and development of various cancers. Recent studies have shown that aberrant m(6)A regulators and m(6)A levels have dual effects on cancer progression, acting as both promoters and inhibitors. Additionally, direct interactions between different m(6)A regulators and mRNAs have been observed in various cancers. This review summarizes the functions of m(6)A regulators and their roles in different types of cancers, and discusses the potential clinical applications of targeting m(6)A regulators.
m(6)A modification, the most abundant and widespread RNA modification, is present and involved in the occurrence and development of various cancers. To date, most studies have mainly focused on the roles of a single m(6)A regulator (writer/eraser/reader) in various cancers, but cumulative evidence shows that aberrant m(6)A regulators and m(6)A levels exert dual effects (promoting and/or inhibiting roles) in cancer progression. Recently, studies have investigated the direct interactions between different m(6)A regulators (writer/eraser and reader) and mRNAs in a variety of cancers. In this review, we summarize the functions of m(6)A regulators and their roles in various types of cancers. We further propose the possible crosstalk mechanisms (Writer-m(6)A-Reader-mRNA axis and Eraser-m(6)A-Reader-mRNA axis) between different m(6)A regulators and mRNAs during cancer progression. We also discuss the clinical potential of m(6)A regulator-targeting strategies.

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