Abstract
Modification of m6A, as the most abundant mRNA modification, plays diverse roles in various biological processes in eukaryotes. Emerging evidence has revealed that m6A modification is closely associated with the activation and inhibition of tumor pathways, and it is significantly linked to the prognosis of cancer patients. Aberrant reduction or elevated expression of m6A regulators and of m6A itself have been identified in numerous tumors. In this review, we give a description of the dynamic properties of m6A modification regulators, such as methyltransferases, demethylases, and m6A binding proteins, and indicate the value of the balance between these proteins in regulating the expression of diverse genes and the underlying effects on cancer development. Furthermore, we summarize the “dual-edged weapon” role of RNA methylation in tumor progression and discuss that RNA methylation can not only result in tumorigenesis but also lead to suppression of tumor formation. In addition, we summarize the latest research progress on small-molecule targeting of m6A regulators to inhibit or activate m6A. These studies indicate that restoring the balance of m6A modification via targeting specific imbalanced regulators may be a novel anti-cancer strategy.
Highlights
To date, various post-transcriptional RNA modifications have been identified in almost all living organisms (1)
This review summarizes the phenomenon that RNA methylation triggers or suppresses tumor formation and the latest studies on the application of small molecules targeting m6A regulators in various types of tumors
The importance of m6A modification has gradually been discovered by increasing numbers of studies
Summary
Various post-transcriptional RNA modifications have been identified in almost all living organisms (1). How m6A influences tumorigenesis by regulating targeted genes relies on three factors: (1) whether the targeted genes act as oncogenes or anti-oncogenes, (2) the levels of m6A in the cancer (depending on the activity or relative expression level of writers and/or erasers), and (3) the alteration of target mRNA after methylation (which relies on readers) Given these vital factors, the role of m6A in cancer is not easy to elucidate. M6A-seq data identified that ALKBH5 interacts and co-localizes with FOXM1, which plays a necessary role in promoting tumorigenicity in GBM (68) These results demonstrate that tumorigenesis in GSC is negatively correlated with the general m6A modification level, indicating that the reduction of m6A RNA methylation, confirmed by either the knock-down of writers (METTL3/14) or overexpression of erasers (ALKBH5), significantly enhances the growth of tumors. A study showed that m6A modification was often upregulated in GSCs
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