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Updated: Jun 23, 2025

A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues
08:56

A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues

Published on: December 5, 2016

10.9K

Insight into the regulatory mechanism of m6A modification: From MAFLD to hepatocellular carcinoma

Xuan Zha1, Zewei Gao2, Min Li2

  • 1Department of Laboratory Medicine, the Affiliated Hospital of Jiangsu University, Zhenjiang, China; Department of Immunology, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|June 21, 2024
PubMed

Insights

Metabolic-associated fatty liver disease (MAFLD) is rising globally. This review explores how N6-methyladenosine (m6A) modification impacts MAFLD progression to liver cancer and its therapeutic potential.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Oncology

Background:

  • Metabolic-associated fatty liver disease (MAFLD) incidence is increasing globally, linked to obesity and type 2 diabetes mellitus (T2DM).
  • MAFLD affects over one-third of adults worldwide, becoming the most common liver disease.
  • MAFLD is a significant risk factor for hepatocellular carcinoma (HCC), with a notable percentage of HCC cases arising directly from MAFLD without cirrhosis.

Purpose of the Study:

  • To investigate the role of N6-methyladenosine (m6A) modification in the progression of MAFLD to HCC.
  • To explore the potential of targeting m6A as a therapeutic strategy for MAFLD-related HCC.
  • To identify future research directions concerning m6A in MAFLD-HCC transition.

Main Methods:

  • Review of existing literature on m6A modification, MAFLD, and HCC.
  • Analysis of studies linking aberrant m6A patterns to metabolic alterations and cancer development.
  • Synthesis of current understanding regarding m6A's impact on MAFLD pathogenesis and HCC transformation.

Main Results:

  • Abnormal m6A modification is closely associated with cellular metabolic dysregulation, contributing to MAFLD onset and progression.
  • Evidence suggests a critical role for m6A in the direct transformation of MAFLD to HCC.
  • The precise mechanisms by which m6A influences MAFLD-to-HCC transition require further elucidation.

Conclusions:

  • Aberrant m6A modification is implicated in the progression of MAFLD to HCC.
  • Targeting m6A pathways presents a promising therapeutic avenue for MAFLD-related HCC.
  • Further research is warranted to fully understand and exploit m6A's role in MAFLD-associated liver cancer.
Keywords:
Hepatocellular carcinomaImmunotherapyMetabolic-associated fatty liver diseaseN6-methyladenosine

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