Epigenetic modification of m6A regulator proteins in cancer
Yumin Wang, Yan Wang, Harsh Patel, Jichao Chen, Jinhua Wang, Zhe‐Sheng Chen, Hongquan Wang
Abstract
Abstract Divergent N 6 -methyladenosine (m 6 A) modifications are dynamic and reversible posttranscriptional RNA modifications that are mediated by m 6 A regulators or m 6 A RNA methylation regulators, i.e., methyltransferases (“writers”), demethylases (“erasers”), and m 6 A-binding proteins (“readers”). Aberrant m 6 A modifications are associated with cancer occurrence, development, progression, and prognosis. Numerous studies have established that aberrant m 6 A regulators function as either tumor suppressors or oncogenes in multiple tumor types. However, the functions and mechanisms of m 6 A regulators in cancer remain largely elusive and should be explored. Emerging studies suggest that m 6 A regulators can be modulated by epigenetic modifications, namely, ubiquitination, SUMOylation, acetylation, methylation, phosphorylation, O-GlcNAcylation, ISGylation, and lactylation or via noncoding RNA action, in cancer. This review summarizes the current roles of m 6 A regulators in cancer. The roles and mechanisms for epigenetic modification of m 6 A regulators in cancer genesis are segregated. The review will improve the understanding of the epigenetic regulatory mechanisms of m 6 A regulators.