Mechanism of RNA modification N6-methyladenosine in human cancer

Since the breakthrough discoveries of DNA and histone modifications, the field of RNA modifications has gained increasing interest in the scientific community. The discovery of N6-methyladenosine (m6A), a predominantly internal epigenetic modification in eukaryotes mRNA, heralded the creation of the...

Full description

Saved in:
Bibliographic Details
Published inMolecular cancer Vol. 19; no. 1; pp. 104 - 20
Main Authors Zhou, Zijian, Lv, Jiancheng, Yu, Hao, Han, Jie, Yang, Xiao, Feng, Dexiang, Wu, Qikai, Yuan, Baorui, Lu, Qiang, Yang, Haiwei
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 08.06.2020
BioMed Central
BMC
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Since the breakthrough discoveries of DNA and histone modifications, the field of RNA modifications has gained increasing interest in the scientific community. The discovery of N6-methyladenosine (m6A), a predominantly internal epigenetic modification in eukaryotes mRNA, heralded the creation of the field of epi-transcriptomics. This post-transcriptional RNA modification is dynamic and reversible, and is regulated by methylases, demethylases and proteins that preferentially recognize m6A modifications. Altered m6A levels affect RNA processing, degradation and translation, thereby disrupting gene expression and key cellular processes, ultimately resulting in tumor initiation and progression. Furthermore, inhibitors and regulators of m6A-related factors have been explored as therapeutic approaches for treating cancer. In the present review, the mechanisms of m6A RNA modification, the clinicopathological relevance of m6A alterations, the type and frequency of alterations and the multiple functions it regulates in different types of cancer are discussed.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
ISSN:1476-4598
1476-4598
DOI:10.1186/s12943-020-01216-3