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Review
. 2020 May 12;19(1):88.
doi: 10.1186/s12943-020-01204-7.

The potential role of RNA N6-methyladenosine in Cancer progression

Affiliations
Review

The potential role of RNA N6-methyladenosine in Cancer progression

Tianyi Wang et al. Mol Cancer. .

Abstract

N6-methyladenosine (m6A) is considered the most common, abundant, and conserved internal transcript modification, especially in eukaryotic messenger RNA (mRNA). m6A is installed by m6A methyltransferases (METTL3/14, WTAP, RBM15/15B, VIRMA and ZC3H13, termed "writers"), removed by demethylases (FTO, ALKBH5, and ALKBH3, termed "erasers"), and recognized by m6A-binding proteins (YTHDC1/2, YTHDF1/2/3, IGF2BP1/2/3, HNRNP, and eIF3, termed "readers"). Accumulating evidence suggests that m6A RNA methylation greatly impacts RNA metabolism and is involved in the pathogenesis of many kinds of diseases, including cancers. In this review, we focus on the physiological functions of m6A modification and its related regulators, as well as on the potential biological roles of these elements in human tumors.

Keywords: Cancer progression; Molecular mechanisms; N6-methyladenosine (m6A).

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
The molecular mechanism of m6A mutation. m6A is installed by “writers” (METTL3/14, WTAP, RBM15/15B, VIRMA and ZC3H13), removed by “erasers” (FTO, ALKBH5, and ALKBH3, termed “erasers”), and recognized by “readers” (YTHDC1/2, YTHDF1/2/3, IGF2BP1/2/3, HNRNP, and eIF3, termed “readers”)
Fig. 2
Fig. 2
The detailed molecular mechanism of m6A enzymes. The “writers”, “erasers” and “readers” relay on various related factors install, remove and recognize m6A mutation and affect RNA metabolic processes, including RNA splicing, export, translation, degradation and so on
Fig. 3
Fig. 3
The potential roles of m6A in cancer progression. The potential role of m6A in cancer progression is reflected in the regulation of tumor-associated gene expression. m6A modification promotes cancer progression by enhancing oncogene expression and inhibiting tumor suppressor gene expression. m6A modification hinders cancer progression by inhibiting oncogene expression and enhancing tumor suppressor gene expression

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