ArticleOncogene2007
Helicobacter pylori CagA interacts with E-cadherin and deregulates the beta-catenin signal that promotes intestinal transdifferentiation in gastric epithelial cells.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 253 papers, 3 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
253 citing papers in PubMed, 3 syntheses or guidelines pooled it, 456 citations in OpenAlex.
- Infiltration to infection: key virulence players of Helicobacter pylori pathogenicity.Infection · 2024Pooled it
- A meta-analysis of abnormal β-catenin immunohistochemical expression as a prognostic factor in lung cancer: location is more important.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016Pooled it
- Abnormal β-catenin immunohistochemical expression as a prognostic factor in gastric cancer: a meta-analysis.World journal of gastroenterology · 2014Pooled it
- Dietary PUFA Increase Apoptosis in Stomach of Patients with Dyspeptic Symptoms and Infected with H. pylori.Lipids · 2017Trial
- Host andGut microbes · 2026Article
- A model of Helicobacter infection using an artificial liver constructed by a radial-flow bioreactor.Human cell · 2026Article
- The "Hit-and-Run" legacy: epigenetic locking and the survival switch in H. pylori-associated gastric cancer.Cell death discovery · 2026Review
- Spatial transcriptomics defines IM-crypt as a premalignant niche with bidirectional divergence in early gastric carcinogenesis.Communications biology · 2026Article
- Genotoxic Bacteria and Oncogenic Viruses in Colorectal Cancer: Evidence, Gaps, and a Proposed Interaction Model.International journal of molecular sciences · 2026Review
- Rethinking the microenvironment's role in chemical-induced malignancy.Toxicological sciences : an official journal of the Society of Toxicology · 2026Review
- Taurine suppresses gastric intestinal metaplasia in patient-derived organoids andWorld journal of gastrointestinal oncology · 2026Article
- Microbiome modulation of tumorigenesis and immune responses.Journal of biomedical science · 2026Review
- The relationship between gut microbiota and cancer immune response and immunotherapy.Frontiers in immunology · 2026Review
- Article
- Update on the pathogenesis and clinical management ofWorld journal of gastrointestinal pathophysiology · 2025Review
- Nuclear β-catenin: molecular regulation, challenges and therapeutic opportunities.Cell communication and signaling : CCS · 2025Review
- Gastrointestinal cancer: molecular pathogenesis and targeted therapy.Molecular biomedicine · 2025Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Microbiome-targeted nanoplatforms and engineering approaches in breast cancer therapy.Molecular cancer · 2025Review
- Review
193 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
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with Helicobacter pylori cagA-positive strains is associated with gastric adenocarcinoma. Intestinal metaplasia is a precancerous lesion of the stomach characterized by transdifferentiation of the gastric mucosa to an intestinal phenotype. The H. pylori cagA gene product, CagA, is delivered into gastric epithelial cells, where it undergoes tyrosine phosphorylation by Src family kinases. Tyrosine-phosphorylated CagA specifically binds to and activates SHP-2 phosphatase, thereby inducing cell-morphological transformation. We report here that CagA physically interacts with E-cadherin independently of CagA tyrosine phosphorylation. The CagA/E-cadherin interaction impairs the complex formation between E-cadherin and beta-catenin, causing cytoplasmic and nuclear accumulation of beta-catenin. CagA-deregulated beta-catenin then transactivates beta-catenin-dependent genes such as cdx1, which encodes intestinal specific CDX1 transcription factor. In addition to beta-catenin signal, CagA also transactivates p21(WAF1/Cip1), again, in a phosphorylation-independent manner. Consequently, CagA induces aberrant expression of an intestinal-differentiation marker, goblet-cell mucin MUC2, in gastric epithelial cells that have been arrested in G1 by p21(WAF1/Cip1). These results indicate that perturbation of the E-cadherin/beta-catenin complex by H. pylori CagA plays an important role in the development of intestinal metaplasia, a premalignant transdifferentiation of gastric epithelial cells from which intestinal-type gastric adenocarcinoma arises.
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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.