ArticleCell death & disease2025
Hypermethylation-mediated HNF4A silencing by Helicobacter pylori infection drives gastric cancer by disrupting epithelial cell polarity and activating EMT signaling.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Article
- Pan-cancer expression, methylation, and prognostic significance of α7 nicotinic acetylcholine receptor in tumor immunology.Biochemistry and biophysics reports · 2026Article
- Vascular SMC-like CAF-derived THBS1 drives tumor-associated neutrophil recruitment to orchestrate an immunosuppressive microenvironment in gastric cancer.Cell death & disease · 2026Article
- The role of HNF4α in adenocarcinoma.Biochemical Society transactions · 2026Review
- TYMP upregulation mediated by the hyperactivated IL-17/NF-κB1 axis promotes psoriasis through enhancing aberrant keratinization and neutrophil-mediated inflammation.Biology direct · 2026Article
- Helicobacter pylori-linked gene CFAP73 rewires epithelial programs and shapes the gastric cancer microenvironment.Discover oncology · 2026Article
- Engineered mesenchymal stem cells expressing CXCR4 and LIGHT enhance Anti-Tumor activity in a subcutaneous gastric cancer xenograft model.Medical oncology (Northwood, London, England) · 2026Article
- Chronic inflammation promotes gastric cancer progression via ADAM10-mediated cleavage of CX3CL1.Scientific reports · 2026Article
- Rethinking gastric carcinogenesis: a multiscale ecological model of risk beyondFrontiers in microbiology · 2026Review
- Silencing TMEM105 suppresses gastric cancer cell growth and migration via proliferation-associated pathways.BMC cancer · 2025Article
- Article
- EHBMT, a method for visualizing tumor evolution, identifies a surge in gastric cancer with hybrid epithelial-mesenchymal phenotypes due to an inflammatory microenvironment.Experimental & molecular medicine · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Helicobacter pylori (Hp.) infection is one of the high-risk factors for gastric carcinogenesis (GC). However, the underlying mechanism remains largely unclear. In this study, we uncover an essential role of Hp. infection in mediating tumor suppressor gene silencing in gastric epithelial cells through promoter DNA hypermethylation. Hepatocyte nuclear factor HNF4A was downregulated in GC and predicted poor survival. The in vitro and in vivo assays together confirmed that HNF4A plays a tumor suppressive role in GC. Single-cell analysis showed that HNF4A was selectively expressed in gastric epithelial cells. Besides, the reduced HNF4A expression in GC was due to promoter DNA hypermethylation. More importantly, we have provided strong evidence that Hp. infection causes HNF4A down-regulation by hypermethylation of its gene promoter. Meanwhile, silencing of HNF4A resulted in loss of epithelial polarity and activation of TGFβ-induced EMT signaling in gastric epithelial cells by transcriptionally regulating the expression of downstream target genes. In addition, the rescue assays indicated that Hp. infection activated EMT signaling of gastric epithelial cells in a HNF4A-dependent manner, thereby driving gastric tumorigenesis and metastasis. In conclusion, HNF4A is a tumor suppressor gene in GC. Hp. infection causes silence of the HNF4A gene by hypermethylation of its promoter, which then disrupts epithelial polarity and induces EMT signaling in gastric epithelial cells, thereby driving gastric tumorigenesis and metastasis.
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