ArticleDigestive diseases and sciences2015
Helicobacter pylori Infection Activates the Akt-Mdm2-p53 Signaling Pathway in Gastric Epithelial Cells.
Article in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Akt Signaling Pathway Is Activated in the Minor Salivary Glands of Patients with Primary Sjögren's Syndrome.International journal of molecular sciences · 2021Trial
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- Study of the relationships among known virulence genes, coccoid transformation and cytotoxicity ofVirulence · 2024Article
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- Dying to Survive-The p53 Paradox.Cancers · 2021Review
- Manifold role of ubiquitin in Helicobacter pylori infection and gastric cancer.Cellular and molecular life sciences : CMLS · 2021Review
- Article
- The Role and Clinical Implications of the Retinoblastoma (RB)-E2F Pathway in Gastric Cancer.Frontiers in oncology · 2021Review
- Targeting MDM2 for novel molecular therapy: Beyond oncology.Medicinal research reviews · 2020Review
- FAM3B promotes progression of oesophageal carcinoma via regulating the AKT-MDM2-p53 signalling axis and the epithelial-mesenchymal transition.Journal of cellular and molecular medicine · 2019Article
- Article
- p53, a potential predictor of Helicobacter pylori infection-associated gastric carcinogenesis?Oncotarget · 2016Review
- Nucleolus-derived mediators in oncogenic stress response and activation of p53-dependent pathways.Histochemistry and cell biology · 2016Review
- Low-dose radiation prevents type 1 diabetes-induced cardiomyopathy via activation of AKT mediated anti-apoptotic and anti-oxidant effects.Journal of cellular and molecular medicine · 2016Article
- Article
- Microbial Regulation of p53 Tumor Suppressor.PLoS pathogens · 2015Review
- Bacterial Pathogen Helicobacter pylori: A Bad AKTor Inhibits p53 Protein Activity [corrected].Digestive diseases and sciences · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUNDS AND
aimsAlthough Helicobacter pylori is widely accepted as a causative factor of many gastric diseases, the signaling pathways affected by H. pylori and subsequent effects on cell apoptosis and proliferation remain unclear. Here, we investigated the molecular mechanisms mediating H. pylori infection in gastric epithelial cells.
methodsTissues from 160 patients with various gastric diseases with or without H. pylori infection were obtained and analyzed by immunohistochemistry for Akt, pAkt, Mdm2, p53, and Bax expression. In vitro, human gastric epithelial cells, GES-1, were incubated with H. pylori culture filtrates. Cell viability was measured by MTT assay. Apoptosis was evaluated by Annexin V/PI double staining followed by flow cytometry, DNA electrophoresis, and comet assay. mRNA and protein expression was assessed by RT-PCR and Western blot analysis.
resultsIn patient tissues, H. pylori infection was associated with significantly elevated levels of pAkt in chronic nonatrophic gastritis (CNAG), Mdm2 in dysplasia, p53 in metaplastic atrophy (MA), and Bax in CNAG and MA. In vitro, H. pylori culture filtrates reduced GES-1 cell viability in a time- and dose-dependent manner, induced G0/G1 arrest, triggered apoptosis, and increased DNA fragmentation. Mdm2 and Bax mRNA expression and pAkt, Mdm2, p53, and Bax protein expression were significantly upregulated when treated with H. pylori culture filtrates. Akt inhibition by LY294002 decreased Mdm2 expression, upregulated p53, and enhanced H. pylori-induced growth inhibition of GES-1 cells.
conclusionsThese findings suggest that Akt-Mdm2-p53 signaling is involved in the molecular response of GES-1 cells to H. pylori infection.
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