4.7 Review

The emerging roles of N6-methyladenosine (m6A) deregulation in liver carcinogenesis

Journal

MOLECULAR CANCER
Volume 19, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12943-020-01172-y

Keywords

Hepatocellular carcinoma; N6-methyladenosine; RNA epigenetics; Epi-transcriptome

Funding

  1. Hong Kong Research Grants Council (RGC) General Research Fund [17142516]
  2. Hong Kong Research Grants Council (RGC) Theme Based Research Scheme [T12-704/16R]

Ask authors/readers for more resources

Liver cancer is a common cancer worldwide. Although the etiological factors of liver carcinogenesis are well defined, the underlying molecular mechanisms remain largely elusive. Epigenetic deregulations, such as aberrant DNA methylation and histone modifications, play a critical role in liver carcinogenesis. Analogous to DNA and core histone proteins, reversible chemical modifications on mRNA have recently been recognized as important regulatory mechanisms to control gene expression. N6-methyladenosine (m6A) is the most prevalent internal mRNA modification in mammalian cells. m6A modification is important for controlling many cellular and biological processes. Deregulation of m6A modification has been recently implicated in human carcinogenesis, including liver cancer. In this review, we summarize the recent findings on m6A regulation and its biological impacts in normal and cancer cells. We will focus on the deregulation of m6A modification and m6A regulators in liver diseases and liver cancers. We will highlight the clinical relevance of m6A deregulation in liver cancer. We will also discuss the potential of exploiting m6A modification for cancer diagnosis and therapeutics.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available