Abstract
N6-methyladenosine (m6A) is regarded as the most abundant, prevalent and conserved internal mRNA modification in mammalian cells. M6A can be catalyzed by m6A methyltransferases METTL3, METTL14 and WTAP (writers), reverted by demethylases ALKBH5 and FTO (erasers), and recognized by m6A -binding proteins such as YTHDF1/2/3, IGF2BP1/2/3 and HNRNPA2B1 (readers). Emerging evidence suggests that m6A modification is significant for regulating many biological and cellular processes and participates in the pathological development of various diseases, including tumors. This article reviews recent studies on the biological function of m6A modification and the methylation modification of m6A in urological tumors.
Highlights
In past decades, epigenetic modification has been identified to be involved in diverse biological processes and disease progression, attracting more and more attention
methyltransferase complex (MTC) has been identified to regulate the installation of m6A and Methyltransferase-like 3 (METTL3), METTL14, and Wilms tumor 1-associated protein (WTAP) have been proved as the core components of this complex (Ping et al, 2014; Schwartz et al, 2014; Zhou J. et al, 2015)
METTL14 can inhibit colorectal cancer (CRC) cell proliferation, migration and invasion via the miR-375-YAP1/SP1 signal axis (Chen X. et al, 2020). Both of METTL3 and METTL14 could act as m6A “writer”, METTL3 might promote the progression of CRC, while METTL14 functions as a tumor suppressor in CRC
Summary
Epigenetic modification has been identified to be involved in diverse biological processes and disease progression, attracting more and more attention. The methyltransferase complex (MTC) can catalyze m6A, demethylase can remove m6A, while RNA reader proteins can recognize m6A and bind to the RNA These proteins play an essential biological role in m6A modifications (Table 1, Figure 1). MTC has been identified to regulate the installation of m6A and Methyltransferase-like 3 (METTL3), METTL14, and Wilms tumor 1-associated protein (WTAP) have been proved as the core components of this complex (Ping et al, 2014; Schwartz et al, 2014; Zhou J. et al, 2015). METTL14 can inhibit CRC cell proliferation, migration and invasion via the miR-375-YAP1/SP1 signal axis (Chen X. et al, 2020) Both of METTL3 and METTL14 could act as m6A “writer”, METTL3 might promote the progression of CRC, while METTL14 functions as a tumor suppressor in CRC. Interacts with RNA helicase and increases the translation efficiency of target RNA
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