ArticleCellular microbiology2009
Helicobacter pylori activate epidermal growth factor receptor- and phosphatidylinositol 3-OH kinase-dependent Akt and glycogen synthase kinase 3beta phosphorylation.
Article in Cellular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 95 citations in OpenAlex.
- Probiotics ameliorate H. pylori-associated gastric β-catenin and COX-2 carcinogenesis signaling by regulating miR-185.Journal of biomedical science · 2025Trial
- Loss of L1CAM from gastric epithelial cells and extracellular vesicles promotes Helicobacter pylori-driven cancer progression and invasiveness.Cell communication and signaling : CCS · 2026Article
- The intratumoral microbiome: a review of the tumor microenvironment's fourth axis shaping anti-tumor immunity, cancer prognosis, and therapeutic response.Frontiers in immunology · 2026Review
- Unveiling a novel model of cell senescence-related genes for prognostic assessment and immunotherapeutic insights in gastric cancer.Scientific reports · 2025Article
- Current Knowledge about Gastric Microbiota with Special Emphasis onCurrent issues in molecular biology · 2024Review
- GRB7-mediated enhancement of cell malignant characteristics induced byFrontiers in microbiology · 2024Article
- Review
- A review of signal pathway induced by virulent protein CagA ofFrontiers in cellular and infection microbiology · 2023Review
- Molecular mechanisms underlying the action of carcinogens in gastric cancer with a glimpse into targeted therapy.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- The JMJD Family Histone Demethylases in Crosstalk Between Inflammation and Cancer.Frontiers in immunology · 2022Review
- Epigenetic Regulation of Inflammatory Signaling and Inflammation-Induced Cancer.Frontiers in cell and developmental biology · 2022Review
- Bacteria-Cancer Interface: Awaiting the Perfect Storm.Pathogens (Basel, Switzerland) · 2021Review
- Metformin attenuates synergic effect of diabetes mellitus and Helicobacter pylori infection on gastric cancer cells proliferation by suppressing PTEN expression.Journal of cellular and molecular medicine · 2021Article
- Review
- MicroRNA Modulation of Host Immune Response and Inflammation Triggered byInternational journal of molecular sciences · 2021Review
- Integrating Network Pharmacology and Experimental Validation to Investigate the Mechanisms of Huazhuojiedu Decoction to Treat Chronic Atrophic Gastritis.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Article
- Mycoplasma hyorhinis infection promotes gastric cancer cell motility via β-catenin signaling.Cancer medicine · 2019Article
- The Possible Role ofFrontiers in oncology · 2019Review
- Bacterial infections and cancer.EMBO reports · 2018Review
2 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
3 authors at 1 institution in 1 country.
Funding
Abstract
The signalling pathways leading to the development of Helicobacter pylori-induced gastric cancer remain poorly understood. We tested the hypothesis that H. pylori infections involve the activation of Akt signalling in human gastric epithelial cancer cells. Immunoblot, immunofluorescence and kinase assays show that H. pylori infection of gastric epithelial cells induced phosphorylation of Akt at Ser 473 and Thr 308. Mutations in the H. pylori virulence factor OipA dramatically reduced phosphorylation of Ser 473, while the cag pathogenicity island mutants predominantly inhibited phosphorylation of Thr 308. As the downstream of Akt activation, H. pylori infection inactivated the inactivation of glycogen synthase kinase 3beta at Ser 9 by its phosphorylation. As the upstream of Akt activation, H. pylori infection activated epidermal growth factor receptor (EGFR) at Tyr 992, phosphatidylinositol 3-OH kinase (PI3K) p85 subunit and PI3K-dependent kinase 1 at Ser 241. Pharmacologic inhibitors of PI3K or mitogen-activated protein kinase kinase (MEK), Akt knock-down and EGFR knock-down showed that H. pylori infection induced the activation of EGFR-->PI3K-->PI3K-dependent kinase 1-->Akt-->extracellular signal-regulated kinase signalling pathways, the inactivation of glycogen synthase kinase 3beta and interleukin-8 production. The combined functions of cag pathogenicity island and OipA were necessary and sufficient for full activation of signalling at each level. We propose activation of these pathways as a novel mechanism for H. pylori-mediated carcinogenesis.
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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.