The role of M6A modification in the regulation of tumor-related lncRNAs

N6-methyladenosine (m6A) is the most abundant modification in eukaryotic cells, and it regulates RNA transcription, processing, splicing, degradation, and translation. Long non-coding RNAs (lncRNAs), as transcriptional products with no or limited protein coding ability more than 200 nt in length, pl...

Full description

Saved in:
Bibliographic Details
Published in:Molecular therapy. Nucleic acids Vol. 24; pp. 768 - 779
Main Authors: Lan, Yufei, Liu, Boyang, Guo, Hongbo
Format: Journal Article
Language:English
Published: Elsevier Inc 04-06-2021
American Society of Gene & Cell Therapy
Elsevier
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:N6-methyladenosine (m6A) is the most abundant modification in eukaryotic cells, and it regulates RNA transcription, processing, splicing, degradation, and translation. Long non-coding RNAs (lncRNAs), as transcriptional products with no or limited protein coding ability more than 200 nt in length, play an important role in epigenetic modification, mRNA transcription, splicing, stability, translation, and other biological functions. Extensive studies have shown that both m6A modification and lncRNAs are involved in the pathogenesis of various diseases, such as kinds of cancers, heart failure, Alzheimer’s disease, periodontitis, human abdominal aortic aneurysm, and obesity. To date, m6A modification has been identified as an important biological function in enrichment and regulation of lncRNAs. In this review, we summarize the role of m6A modification in the regulation and function of tumor-related lncRNAs. Moreover, we discuss the potential applications and possible future directions in the field. [Display omitted] In this review, we summarize the role of m6A modification in the regulation and function of tumor-related lncRNAs. Moreover, we discuss the potential applications and possible future directions in the field.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
These authors contributed equally
ISSN:2162-2531
2162-2531
DOI:10.1016/j.omtn.2021.04.002