N6‐methyladenosine (m6A) RNA modification in human cancer

• Published in: Cell proliferation Vol. 53; no. 11; pp. e12921 - n/a
• Main Authors: Huo, Fu‐Chun, Zhu, Zhi‐Man, Pei, Dong‐Sheng
• Format: Journal Article
• Language: English
• Published: Chichester John Wiley & Sons, Inc 01.11.2020; John Wiley and Sons Inc
• Subjects: Biological activity; Biological rhythms; Cancer; Cell division; Eukaryotes; Genes; Homeostasis; Insects; Metabolism; Methylation; MicroRNAs; Molecular modelling; N6-methyladenosine; Pathogenesis; Proteins; Regulatory proteins; Review; Reviews; RNA modification; Stem cells; Tumors
• ISSN: 0960-7722; 1365-2184
• DOI: 10.1111/cpr.12921

N6‐methyladenosine (m6A) RNA modification, first discovered in 1974, is the most prevalent, abundant and penetrating messenger RNA (mRNA) modification in eukaryotes. This governs the fate of modified transcripts, regulates RNA metabolism and biological processes, and participates in pathogenesis of numerous human diseases, especially in cancer through the reciprocal regulation of m6A methyltransferases (“writers”) and demethylases (“erasers”) and the binding proteins decoding m6A methylation (“readers”). Accumulating evidence indicates a complicated regulation network of m6A modification involving multiple m6A‐associated regulatory proteins whose biological functions have been further analysed. This review aimed to summarize the current knowledge on the potential significance and molecular mechanisms of m6A RNA modification in the initiation and progression of cancer. N6‐methyladenosine (m6A) RNA modification in human cancer. m6A modification is a dynamic and reversible process. m6A methylation is catalysed by methyltransferase complexes (writers), reversed by demethylases (erasers) and functionally facilitated by m6A‐binding proteins (readers). m6A methylation participates in carcinogenesis and tumor progression.