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Updated: May 13, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
07:50

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

Published on: September 18, 2020

MYO5B is epigenetically silenced and associated with MET signaling in human gastric cancer

Wenjie Dong1, Liping Wang, Ruizhe Shen

  • 1Department of Internal Medicine-Oncology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.

Digestive Diseases and Sciences
|March 5, 2013
PubMed
Abstract

Insights

Gastric cancer cells epigenetically silence MYO5B via DNA methylation and histone modification. This silencing impacts MET degradation and signaling pathways, revealing a novel mechanism in cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Previous research indicated MYO5B downregulation in gastric cancer.
  • The precise mechanism of MYO5B expression inhibition was previously unknown.

Purpose of the Study:

  • To investigate the epigenetic mechanisms silencing MYO5B in gastric cancer.
  • To elucidate the functional consequences of MYO5B inactivation on MET signaling.

Main Methods:

  • Analysis of the MYO5B promoter CpG island.
  • Methylation-specific PCR (MSP) and bisulfite sequencing (BSP) to assess promoter methylation.
  • ChIP assay to examine histone modifications.
  • Treatment with DNA-demethylating agent (5-aza-2'-deoxycytidine) and histone deacetylase inhibitor (trichostatin A).

Main Results:

  • Aberrant DNA methylation of the MYO5B promoter was confirmed in gastric cancer.
  • Demethylation agents and histone deacetylase inhibitors restored MYO5B expression.
  • MYO5B knockdown in gastric cancer cells led to sustained c-MET levels by inhibiting HGF-stimulated MET degradation.

Conclusions:

  • MYO5B is epigenetically silenced in gastric cancer through DNA methylation and histone modifications.
  • Inactivation of MYO5B affects MET degradation and signaling pathways.
  • This epigenetic silencing represents a novel mechanism in gastric cancer pathogenesis.

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