The dual role of N6-methyladenosine modification of RNAs is involved in human cancers

Abstract

As the most abundant and reversible RNA modification in eukaryotic cells, m⁶ A triggers a new layer of epi-transcription. M⁶ A modification occurs through a methylation process modified by "writers" complexes, reversed by "erasers", and exerts its role depending on various "readers". Emerging evidence shows that there is a strong association between m⁶ A and human diseases, especially cancers. Herein, we review bi-aspects of m⁶ A in regulating cancers mediated by the m⁶ A-associated proteins, which exert vital and specific roles in the development of various cancers. Generally, the m⁶ A modification performs promotion or inhibition functions (dual role) in tumorigenesis and progression of various cancers, which suggests a new concept in cancer regulations. In addition, m⁶ A-targeted therapies including competitive antagonists of m⁶ A-associated proteins may provide a new tumour intervention in the future.

Keywords: ALKBH5; FTO; METTL3; N6-methyladenosine (m6A); cancer; epigenetics.