N-methyladenosine (mA) is the most common post-transcriptional RNA modification throughout the transcriptome, affecting fundamental aspects of RNA metabolism. mA modification could be installed by mA "writers" composed of core catalytic components (METTL3/METTL14/WTAP) and newly defined regulators and removed by mA "erasers" (FTO and ALKBH5). The function of mA is executed by mA "readers" that bind to mA directly (YTH domain-containing proteins, eIF3 and IGF2BPs) or indirectly (HNRNPA2B1). In the past few years, advances in mA modulators ("writers," "erasers," and "readers") have remarkably renewed our understanding of the function and regulation of mA in different cells under normal or disease conditions. However, the mechanism and the regulatory network of mA are still largely unknown. Moreover, investigations of the mA physiological roles in human diseases are limited. In this review, we summarize the recent advances in mA research and highlight the functional relevance and importance of mA modification in in vitro cell lines, in physiological contexts, and in cancers.
Adenosine ; analogs & derivatives ; metabolism ; Cell Differentiation ; physiology ; Humans ; Neoplasms ; metabolism ; RNA ; metabolism ; RNA Processing, Post-Transcriptional