ArticleCell communication and signaling : CCS2024
Gamma-glutamyl transferase secreted by Helicobacter pylori promotes the development of gastric cancer by affecting the energy metabolism and histone methylation status of gastric epithelial cells.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- From Gene to Enzyme: Multidimensional Decoding of the GGT Molecular Family and Its Clinical Tumor Diagnosis.Cancer medicine · 2025Pooled it
- Associations of bilirubin, albumin, and the ALBI index with gastric cancer risk: a smoking-stratified prospective cohort study in men.BMC gastroenterology · 2026Article
- Hijacked epigenomes: how bacterial effectors rewrite host gene expression.Archives of microbiology · 2026Review
- Article
- From Tumor Biology to Clinical Perspectives: Novel Biomarkers and Therapeutic Insights in Gastric Cancer.Oncology research · 2026Review
- Artificial intelligence in gastric cancer research: a bibliometric and visualized analysis from 1993 to 2026.Frontiers in oncology · 2026Review
- Metabolic reprogramming as a key regulator in Helicobacter pylori-infected gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Review
- The interplay of the microbiome, host genetics, and epigenetic modifications in gastric cancer.Frontiers in microbiology · 2026Review
- Mucosal vaccination with enzymatically activeFrontiers in microbiology · 2026Article
- Helicobacter pylori activates DOPEY1 to promote p53 degradation through the USP7/TRIP12 axis in gastric tumorigenesis.Oncogene · 2025Article
- Hotspots and trends in gastric cancer stem cell research: a visualization and bibliometric analysis.Frontiers in oncology · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundHelicobacter pylori (H. pylori) infection is critical in the development and occurrence of gastric cancer. H. pylori secretes gamma-glutamyl transferase (GGT), which affects energy metabolism and histone methylation in mesenchymal stem cells. However, its effect on human gastric epithelial cells remains unclear. This study aimed to investigate the effects of GGT on energy metabolism and histone methylation in gastric epithelial cells and determine its role in the development and progression of H. pylori-induced gastric cancer.
methodsA GGT knockout H. pylori strain and mouse gastric cancer model were constructed, and alpha-ketoglutarate (α-KG) was added. The underlying mechanism was investigated using proteomics, immunohistochemistry, Western blotting, and other experimental assays.
resultsH. pylori can colonize the host's stomach and destroy the gastric epithelium. GGT secreted by H. pylori decreased the concentration of glutamine in the stomach and increased H3K9me3 and H3K27me3 expression, which promoted the proliferation and migration of gastric epithelial cells. Additionally, α-KG reversed this effect. GGT increased the tumorigenic ability of nude mice. GGT, secreted by H. pylori, promoted the expression of ribosomal protein L15 (RPL15), while GGT knockout and supplementation with α-KG and trimethylation inhibitors reduced RPL15 expression and Wnt signaling pathway expression.
conclusionsH. pylori secreted GGT decreased the expression of glutamine and α-KG in gastric epithelial cells, increased the expression of histones H3K9me3 and H3K27me3, and activated the Wnt signaling pathway through RPL15 expression, ultimately changing the biological characteristics of the gastric epithelium and promoting the occurrence of gastric cancer. Altered energy metabolism and histone hypermethylation are important factors involved in this process.
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