It's complicated… m6A-dependent regulation of gene expression in cancer

Biochim Biophys Acta Gene Regul Mech. 2019 Mar;1862(3):382-393. doi: 10.1016/j.bbagrm.2018.09.010. Epub 2018 Oct 5.

Abstract

Cellular function relies on multiple pathways that are coordinated to ensure the proper execution of gene expression networks. Failure to coordinate the multiple programs active in the cell can have catastrophic consequences and lead to diseases such as cancer. At the post-transcriptional level, RNA modifications play important roles in the regulation of gene expression. N6-methyladenosine (m6A) is the most abundant internal messenger RNA (mRNA) modification and has gained increasing interest in the last few years as a dynamic regulator of RNA metabolism. Modifications regulate all stages of the RNA life cycle, from transcription to decay. Recent studies have pointed to the role of RNA methylation in cancer initiation and progression, and aberrant modification has served as a biomarker of early-stage diagnosis in several cancers. Here, we review the regulation of m6A, disruptions to methylation-dependent pathways that influence carcinogenesis, and potential avenues for m6A-related therapeutic strategies.

Keywords: Cancer; Epitranscriptome; Gene regulation; m(6)A.

Publication types

  • Research Support, N.I.H., Intramural
  • Review

MeSH terms

  • Adenine / analogs & derivatives*
  • Adenine / metabolism
  • Animals
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • RNA Processing, Post-Transcriptional*

Substances

  • Adenine
  • 6-methyladenine