Abstract
N(6)-methyladenosine (m(6)A) modification is found the most prevalent and abundant post-transcriptional mRNA modification in eukaryotic cells. It regulates almost all stages of RNA life cycle including splicing, translocation, stability, decay and translation. As a dynamic and reversible process, m(6)A modification is catalyzed by the RNA methyltransferases ('writers'), removed by the demethylases ('erasers'), and interacts with m(6)A-binding proteins ('readers'). Recent studies have revealed that these m(6)A modification regulators are frequently expressed aberrantly in various types of cancer, and involved in cell proliferation, differentiation, metabolism, particularly, in tumorigenesis and tumor progression through diverse mechanisms. In this review, the m(6)A modification process and its regulatory functions in lung cancer are summarized. Furthermore, the research progress in the inhibitor development of m(6)A modification, and the potential of targeting m(6)A modifying proteins for clinical application are discussed.