| Literature DB >> 33611339 |
Xiulin Jiang1,2, Baiyang Liu1,2, Zhi Nie1,2,3, Lincan Duan3, Qiuxia Xiong3, Zhixian Jin3, Cuiping Yang4, Yongbin Chen5,6.
Abstract
N6-methyladenosine (m6A) is the most prevalent, abundant and conserved internal cotranscriptional modification in eukaryotic RNAs, especially within higher eukaryotic cells. m6A modification is modified by the m6A methyltransferases, or writers, such as METTL3/14/16, RBM15/15B, ZC3H3, VIRMA, CBLL1, WTAP, and KIAA1429, and, removed by the demethylases, or erasers, including FTO and ALKBH5. It is recognized by m6A-binding proteins YTHDF1/2/3, YTHDC1/2 IGF2BP1/2/3 and HNRNPA2B1, also known as "readers". Recent studies have shown that m6A RNA modification plays essential role in both physiological and pathological conditions, especially in the initiation and progression of different types of human cancers. In this review, we discuss how m6A RNA methylation influences both the physiological and pathological progressions of hematopoietic, central nervous and reproductive systems. We will mainly focus on recent progress in identifying the biological functions and the underlying molecular mechanisms of m6A RNA methylation, its regulators and downstream target genes, during cancer progression in above systems. We propose that m6A RNA methylation process offer potential targets for cancer therapy in the future.Entities:
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Year: 2021 PMID： 33611339 PMCID： PMC7897327 DOI： 10.1038/s41392-020-00450-x
Source DB: PubMed Journal: Signal Transduct Target Ther ISSN： 2059-3635