Helicobacter pylori Is Associated with miR-133a Expression through Promoter Methylation in Gastric Carcinogenesis
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Updated: Feb 22, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
Joo Hyun Lim1,2, Sang Gyun Kim2, Ji Min Choi1
1Department of Internal Medicine and Healthcare Research Institute, Healthcare System Gangnam Center, Seoul National University Hospital, Seoul, Korea.
Background/Aims:
To investigate whether Helicobacter pylori eradication can reverse epigenetic silencing of microRNAs (miRNAs) which are associated with H. pylori-induced gastric carcinogenesis.
Methods:
We examined expression and promoter methylation of miR-34b/c, miR-133a, let-7a, and let-7i in gastric cancer cell line, before/after demethylation. Among them, epigenetically controlled miRNAs were identified. Their expression and promoter methylation was examined in human tissues of H. pylori-positive gastric cancer (T), H. pylori-positive gastritis (H), and H. pylori-negative controls (C). We also compared changes of miRNA expression and promoter methylation in H. pylori-positive patients who were endoscopically treated for early gastric cancer, between baseline and 1 year later according to eradication status.
Results:
In gastric cancer cell line, miR-34b/c and miR-133a showed epigenetic silencing. In human tissues, miR-34b/c and miR-133a showed serial increase of promoter methylation in order of C, H, and T (all, p<0.01), and the miR-133a expression showed serial decrease (C vs H, p=0.02; H vs T, p=0.01; C vs T, p<0.01) while miR-34b and miR-34c expressions did not. H. pylori eradication induced decrease of methylation (p<0.01) and increase of miR-133a expression (p=0.03), compared with noneradication group.
Conclusions:
This result suggests H. pylori eradication could reverse methylation-silencing of miR-133a which is involved in H. pylori-induced gastric carcinogenesis.
Insights
Helicobacter pylori eradication can reverse epigenetic silencing of miR-133a, a microRNA (miRNA) involved in gastric cancer. This finding suggests a potential therapeutic strategy for H. pylori-associated gastric carcinogenesis.
Area of Science:
- Epigenetics
- Molecular Biology
- Oncology
Background:
- Helicobacter pylori infection is a major risk factor for gastric cancer.
- Epigenetic silencing of microRNAs (miRNAs) plays a role in H. pylori-induced gastric carcinogenesis.
- Specific miRNAs like miR-133a are implicated in this process.
Purpose of the Study:
- To investigate if H. pylori eradication can reverse the epigenetic silencing of specific miRNAs.
- To determine the role of miR-133a in H. pylori-associated gastric carcinogenesis.
- To assess the impact of H. pylori eradication on miRNA expression and methylation.
Main Methods:
- Examined expression and promoter methylation of miR-34b/c, miR-133a, let-7a, and let-7i in gastric cancer cell lines and human tissues.
- Assessed miRNA changes in H. pylori-positive patients before and after treatment, comparing eradication and non-eradication groups.
- Utilized demethylation in cell lines to identify epigenetically controlled miRNAs.
Main Results:
- miR-133a and miR-34b/c showed epigenetic silencing in gastric cancer cell lines.
- Promoter methylation of miR-34b/c and miR-133a increased progressively from control to gastritis to cancer tissues.
- H. pylori eradication led to decreased miR-133a promoter methylation and increased expression.
Conclusions:
- H. pylori eradication can reverse the methylation-based silencing of miR-133a.
- miR-133a is involved in H. pylori-induced gastric carcinogenesis.
- Targeting epigenetic modifications may offer a therapeutic approach for H. pylori-related gastric cancer.
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