Abstract
N(6)-methyladenosine (m(6)A) is an essential RNA modification that regulates key cellular processes, including stem cell renewal, cellular differentiation, and response to DNA damage. Unsurprisingly, aberrant m(6)A methylation has been implicated in the development and maintenance of diverse human cancers. Altered m(6)A levels affect RNA processing, mRNA degradation, and translation of mRNAs into proteins, thereby disrupting gene expression regulation and promoting tumorigenesis. Recent studies have reported that the abnormal expression of m(6)A regulatory enzymes affects m(6)A abundance and consequently dysregulates the expression of tumor suppressor genes and oncogenes, including MYC, SOCS2, ADAM19, and PTEN. In this review, we discuss the specific roles of m(6)A "writers", "erasers", and "readers" in normal physiology and how their altered expression promotes tumorigenesis. We also describe the potential of exploiting the aberrant expression of these enzymes for cancer diagnosis, prognosis, and the development of novel therapies.