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Review
. 2018 Jul 21;17(1):101.
doi: 10.1186/s12943-018-0847-4.

Novel insights on m6A RNA methylation in tumorigenesis: a double-edged sword

Shaoyun Wang  1 , Peiwei Chai  1 , Ruobing Jia  1 , Renbing Jia  2
Affiliations
Review

Novel insights on m6A RNA methylation in tumorigenesis: a double-edged sword

Shaoyun Wang et al. Mol Cancer. .

Abstract

N6-methyladenosine (m6A), the most prevalent modification of mammalian RNA, has received increasing attention. Although m6A has been shown to be associated with biological activities, such as spermatogenesis modulation, cell spermatogenesis and pluripotency, Drosophila sex determination, and the control of T cell homeostasis and response to heat shock, little is known about its roles in cancer biology and cancer stem cells VSports手机版. Recent articles have noted that some genes have abnormal m6A expression after tumorigenesis, including genes ABS2, RARA, MYB, MYC, ADAM19 and FOX1. Abnormal changes in the m6A levels of these genes are closely related to tumour occurrence and development. In this review, we summarized the 'dual edge weapon' role of RNA methylation in the tumorigenesis. We discussed RNA methylation could lead to not only tumour progression but also tumour suppression. Moreover, we clarified that the abnormal changes in the m6A enrichment of specific loci contribute to tumour occurrence and development, thereby representing a novel anti-cancer strategy by restoration to balanced RNA methylation in tumour cells. .

Keywords: RNA methylation; Tumorigenesis; m6A. V体育安卓版.

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The authors declare that they have no competing interests.

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Figures (V体育官网入口)

Fig. 1
Fig. 1
The process of m6A RNA modification. The installation, removal and identification of m6A are performed by writers, readers, and erasers, respectively. Writers interact with a special sequence of RRACH in mRNA that produces catalytic action mediated by METTL3, METTL14, KIAA1429, ZC3H13, METTL16 and WTAP. m6A functions are received by some reader proteins: YT521-B homology (YTH) domain-containing protein, IGF2BP, FMR1, LRPPRC and the heterogeneous nuclear ribonucleoprotein (HNRNP) protein families. Two m6A eraser proteins are obesity-associated protein (FTO) and alkB homologue 5 (ALKBH5)
Fig. 2
Fig. 2
m6A modification functions as a ‘dual-edged sword’ in tumor progression. In AML, aberrant FTO, METTL14 and METTL3 lead to aberrant expression of the ASB2, RARA, MYC, MYB, BCL2, SP1 and PTEN genes through m6A modification, ultimately promoting tumorigenesis. In GSCs, aberrant METTL3, METTL14 and ALKBH5 lead to the aberrant expression of ADAM19 and FOXM1 through m6A modifications, ultimately promoting tumorigenesis. In HCC, aberrant METTL3 and METTL14 lead to the aberrant expression of SOCS2 and miR126 through m6A modifications, ultimately promoting tumorigenesis. In BCSCs, aberrant METTL3 leads to the aberrant expression of KLF4, NANOG and HBXIP through m6A modifications, ultimately promoting tumorigenesis. In cervical cancer, aberrant FTO leads to the aberrant expression of β-catenin
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