Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Oct 1;8(10):1957-1966.
eCollection 2018.

N6-methyladenine RNA modification and cancers

Xia Wu  1 , Lina Sang  1 , Yuping Gong  1
Affiliations
Review

N6-methyladenine RNA modification and cancers

Xia Wu et al. Am J Cancer Res. .

Abstract

Similar to DNA methylation modifications, N6-methyladenine (m6A) has been identified as a dynamic and reversible modification in messenger RNA (mRNA), regulated by m6A methyltransferases and demethylases. m6A modifications regulate gene expressions and play vital roles in many life processes. Some proteins serve as m6A-binding proteins to perform the m6A-modified biological functions. Recently, m6A modifications have been reported to play critical roles in human cancers, including lung cancer, brain tumor, leukemia, and many others. In this comprehensive review, we have described the roles played by m6A modifications of mRNA in the development of cancers. These modifications appear to have an oncogenic role in some cancers while a tumor-suppressor role in others. Therefore, it would be of great significance to study the biological functions of genes regulated by m6A in different cancers and identify the key m6A target genes to understand the potential mechanism underlying the pathogenesis of cancer.

Keywords: N6-methyladenine (m6A); RNA epigenetics; cancer; demethylases; methyltransferases.

PubMed Disclaimer

Conflict of interest statement

None.

Figures

Figure 1
Figure 1
Cellular pathways of m6A-based modification of RNA. m6A methyltransferase complex METTL3-METTL14-WTAP and m6A demethylases FTO and ALKBH5 dynamically and reversibly regulate the m6A levels in RNA within the nucleus. Nuclear m6A-reader proteins (hnRNPs) affect alternative splicing of pre-mRNA and pre-microRNA. Cytoplasmic m6A-reader proteins (YTHDF1/2/3) are engaged in decay and translation of m6A-containing mRNAs [15]. This figure is adapted from Figure 1 of the paper by Siwei Wang et al. [15].
See this image and copyright information in PMC

References

    1. Ng RK, Gurdon JB. Epigenetic inheritance of cell differentiation status. Cell Cycle. 2008;7:1173–7. - PubMed
    1. Zhang LL, Wu JX. DNA methylation: an epigenetic mechanism for tumorigenesis. Yi Chuan. 2006;28:880–5. - PubMed
    1. Strahl BD, Allis CD. The language of covalent histone modifications. Nature. 2000;403:41–5. - PubMed
    1. Wouters BJ, Delwel R. Epigenetics and approaches to targeted epigenetic therapy in acute myeloid leukemia. Blood. 2016;127:42–52. - PubMed
    1. Li Y, Chen K, Zhou Y, Xiao Y, Deng M, Jiang Z, Ye W, Wang X, Wei X, Li J, Liang J, Zheng Z, Yao Y, Wang W, Li P, Xu B. A new strategy to target acute myeloid leukemia stem and progenitor cells using chidamide, a histone deacetylase inhibitor. Curr Cancer Drug Targets. 2015;15:493–503. - PubMed

LinkOut - more resources