ArticleGastroenterology2010
Regulation of p53 tumor suppressor by Helicobacter pylori in gastric epithelial cells.
Article in Gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 2 of them syntheses that pooled it.
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Who cites it
114 citing papers in PubMed, 2 syntheses or guidelines pooled it, 187 citations in OpenAlex.
- Infiltration to infection: key virulence players of Helicobacter pylori pathogenicity.Infection · 2024Pooled it
- Pooled it
- Akt Signaling Pathway Is Activated in the Minor Salivary Glands of Patients with Primary Sjögren's Syndrome.International journal of molecular sciences · 2021Trial
- The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026Review
- Microbiota-host interaction in colorectal cancer: emerging computational technology, multi-omics integration, and mechanisms.Cancer biology & medicine · 2026Review
- Integrated transcriptomics and molecular docking identify hub genes and statin regulators inFrontiers in cellular and infection microbiology · 2026Article
- Orientia tsutsugamushi modulates p53, the cell cycle, and genotoxicity to maintain its intracellular niche.Nature communications · 2025Article
- Gut microbes and their metabolites in relation to the classic tumor suppressor gene P53: a novel narrative.NPJ biofilms and microbiomes · 2025Review
- Exploring the Shared miRNA-mRNA Signature Network Between Helicobacter pylori Infection and Gastric Cancer: A Comparative Study.Current microbiology · 2025Article
- Effect ofImmunotherapy · 2025Review
- Recent advances in the mechanisms of PD-L1 expression in gastric cancer: a review.Biological research · 2025Review
- Decoding microbial carcinogenic strategies: ubiquitination and SUMO modification.Frontiers in microbiology · 2025Review
- Gut Microbiota-Tumor Microenvironment Interactions: Mechanisms and Clinical Implications for Immune Checkpoint Inhibitor Efficacy in Cancer.Cancer management and research · 2025Review
- The influence ofFrontiers in immunology · 2025Article
- The rise and evolving role ofCurrent research in microbial sciences · 2025Review
- The footprint of gut microbiota in gallbladder cancer: a mechanistic review.Frontiers in cellular and infection microbiology · 2024Review
- Network analysis of H. pylori effect on AGS human gastric adenocarcinoma cells gene expression profile.Gastroenterology and hepatology from bed to bench · 2024Article
- Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- Cross-talk betweenFrontiers in cellular and infection microbiology · 2024Article
- Helicobacter pylori CagA promotes immune evasion of gastric cancer by upregulating PD-L1 level in exosomes.iScience · 2023Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsInfection with the gastric mucosal pathogen Helicobacter pylori is the strongest identified risk factor for distal gastric cancer. These bacteria colonize a significant part of the world's population. We investigated the molecular mechanisms of p53 regulation in H pylori-infected cells.
methodsMongolian gerbils were challenged with H pylori and their gastric tissues were analyzed by immunohistochemistry and immunoblotting with p53 antibodies. Gastric epithelial cells were co-cultured with H pylori and the regulation of p53 was assessed by real-time polymerase chain reaction, immunoblotting, immunofluorescence, and cell survival assays. Short hairpin RNA and dominant-negative mutants were used to inhibit activities of Human Double Minute 2 (HDM2) and AKT1 proteins.
resultsWe found that in addition to previously reported up-regulation of p53, H pylori can also negatively regulate p53 by increasing ubiquitination and proteasomal degradation via activation of the serine/threonine kinase AKT1, which phosphorylates and activates the ubiquitin ligase HDM2. These effects were mediated by the bacterial virulence factor CagA; ectopic expression of CagA in gastric epithelial cells increased phosphorylation of HDM2 along with the ubiquitination and proteasomal degradation of p53. The decrease in p53 levels increased survival of gastric epithelial cells that had sustained DNA damage.
conclusionsH pylori is able to inhibit the tumor suppressor p53. H pylori activates AKT1, resulting in phosphorylation and activation of HDM2 and subsequent degradation of p53 in gastric epithelial cells. H pylori-induced dysregulation of p53 is a potential mechanism by which the microorganism increases the risk of gastric cancer in infected individuals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.