ArticleOncotarget2015
Helicobacter pylori bacteria alter the p53 stress response via ERK-HDM2 pathway.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed.
- AURKA regulates LGR5 in response to Helicobacter Pylori infection by modulating its deubiquitination.Cell death and differentiation · 2026Article
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- Antibacterial Activity of the p53 Tumor Suppressor Protein-How Strong Is the Evidence?International journal of molecular sciences · 2025Review
- SOX9 is regulated by AURKA in response to Helicobacter pylori infection via EIF4E-mediated cap-dependent translation.Cancer letters · 2024Article
- An Overview of Selected Bacterial Infections in Cancer, Their Virulence Factors, and Some Aspects of Infection Management.Biology · 2023Review
- Bacterial-Mediated Tumor Therapy: Old Treatment in a New Context.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Review
- CDK1 bridges NF-κB and β-catenin signaling in response to H. pylori infection in gastric tumorigenesis.Cell reports · 2023Article
- Molecular mechanisms underlying the action of carcinogens in gastric cancer with a glimpse into targeted therapy.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Identification of a Novel p53 Modulator Endowed with Antitumoural and Antibacterial Activity through a Scaffold Repurposing Approach.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Helicobacter pylori-induced DNA double-stranded break in the development of gastric cancer.Cancer science · 2022Review
- Small molecule profiling to define synergistic EGFR inhibitor combinations in head and neck squamous cell carcinoma.Head & neck · 2022Article
- Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far.Frontiers in oncology · 2022Review
- Manifold role of ubiquitin in Helicobacter pylori infection and gastric cancer.Cellular and molecular life sciences : CMLS · 2021Review
- Review
- Isoforms of the p53 Family and Gastric Cancer: A Ménage à Trois for an Unfinished Affair.Cancers · 2021Review
- The Role and Clinical Implications of the Retinoblastoma (RB)-E2F Pathway in Gastric Cancer.Frontiers in oncology · 2021Review
- M1 macrophage dependent-p53 regulates the intracellular survival of mycobacteria.Apoptosis : an international journal on programmed cell death · 2020Article
- P53 and The Immune Response: 40 Years of Exploration-A Plan for the Future.International journal of molecular sciences · 2020Review
- Bacillus licheniformis normalize the ileum microbiota of chickens infected with necrotic enteritis.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
H. pylori infection is the strongest known risk factor for gastric cancer. Inhibition of host tumor suppressor mechanisms by the bacteria underlies the development of this disease. Among the tumor suppressors affected by H. pylori are p53 and E-cadherin, which inhibition has been shown to increase the risk of gastric cancer. In this report, we investigated the interaction between E-cadherin and p53 in H. pylori-infected cells. We found that downregulation of E-cadherin leads to cellular stress and activation of p53. In the setting of H. pylori infection, this mechanism, however, is disrupted. We found that although co-culture of gastric epithelial cells with H. pylori led to downregulation of E-cadherin and cellular stress, it resulted in inhibition of p53, which is mediated by intracellular Erk kinases and HDM2 protein induced by H. pylori. Experimental inhibition of HDM2/p53 interactions restored p53 activity, and decreased survival of infected cells. Collectively, our results revealed that regulation of p53 and E-cadherin is tightly linked through the p53 stress response mechanism that is inhibited by H. pylori via activation of Erk1/2-HDM2-p53 pathway leading to survival of damaged cells. This might be advantageous to the bacteria but may increase the cancer risk.
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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.