The role of Insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) as m6A readers in cancer

RNA can be modified by over 170 types of distinct chemical modifications, and the most abundant internal modification of mRNA in eukaryotes is N6-methyladenosine (m(6)A). The m(6)A modification accelerates mRNA process, including mRNA splicing, translation, transcript stability, export and decay. m(6)A RNA modification is installed by methyltransferase-like proteins (writers), and potentially removed by demethylases (erasers), and this process is recognized by m(6)A-binding proteins (readers). Notably, alterations of m(6)A-modified proteins (writers, erasers and readers) are involved in the tumorigenesis, progression and metastasis. Importantly, the fate of m(6)A-methylated mRNA is mediated mostly through m(6)A readers, and among these readers, insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) are unique RNA-binding proteins (RBPs) that stabilize their targets mRNA via m(6)A modification. In this review, we update the writers, erasers and readers, and their cross-talks in m(6)A modification, and briefly discuss the oncogenic role of IGF2BPs in cancer. Most importantly, we mainly review the up-to-date knowledges of IGF2BPs (IGF2BP1/2/3) as m(6)A readers in an m(6)A-modified manner in cancer progression.

Automated summary

RNA can undergo various chemical modifications, with m(6)A being the most abundant internal modification in eukaryotes. The m(6)A modification plays a crucial role in regulating mRNA processing and is implicated in tumorigenesis. IGF2BPs are unique RNA-binding proteins that stabilize mRNA targets through m(6)A modification and have important implications in cancer progression.