ArticleDisease models & mechanisms2013
H. pylori virulence factor CagA increases intestinal cell proliferation by Wnt pathway activation in a transgenic zebrafish model.
Article in Disease models & mechanisms, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 103 citations in OpenAlex.
- Animal models and pathogenesis of gastric cancer: from premalignant conditions-to-metastasis.Cancer biology & medicine · 2026Review
- Gut microbes and their metabolites in relation to the classic tumor suppressor gene P53: a novel narrative.NPJ biofilms and microbiomes · 2025Review
- Menadione reduces the expression of virulence- and colonization-associated genes inMicrobiology (Reading, England) · 2025Article
- The cancer microbiome.Advances in clinical chemistry · 2025Review
- The Influence of Gastric Microbiota and Probiotics inBiomedicines · 2024Review
- A genome-wide association study in Swedish colorectal cancer patients with gastric- and prostate cancer in relatives.Hereditary cancer in clinical practice · 2024Article
- Metabolic disrupting chemicals in the intestine: the need for biologically relevant models: Zebrafish: what can we learn from this small environment-sensitive fish?FEBS open bio · 2024Review
- Remodeling of the gastric environment inmSystems · 2024Article
- Cellular Senescence, Inflammation, and Cancer in the Gastrointestinal Tract.International journal of molecular sciences · 2023Review
- Mechanism-guided fine-tuned microbiome potentiates anti-tumor immunity in HCC.Frontiers in immunology · 2023Review
- Influence ofWorld journal of clinical oncology · 2022Review
- Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1.PLoS biology · 2022Article
- Helicobacter pylori-induced DNA double-stranded break in the development of gastric cancer.Cancer science · 2022Review
- Biomarker Characterization and Prediction of Virulence and Antibiotic Resistance fromBiomolecules · 2022Review
- The EPIYA-ABCC motif of Helicobacter pylori cagA gene and gastric carcinogenesis in Casablanca population.African health sciences · 2022Article
- The gut microbiota can be a potential regulator and treatment target of bone metastasis.Biochemical pharmacology · 2022Review
- The impact of the human microbiome in tumorigenesis, cancer progression, and biotherapeutic development.BMC microbiology · 2022Review
- Article
- Lipopolysaccharides Enhance Epithelial Hyperplasia and Tubular Adenoma in Intestine-Specific Expression ofBiomedicines · 2021Article
- Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Infection with Helicobacter pylori is a major risk factor for the development of gastric cancer, and infection with strains carrying the virulence factor CagA significantly increases this risk. To investigate the mechanisms by which CagA promotes carcinogenesis, we generated transgenic zebrafish expressing CagA ubiquitously or in the anterior intestine. Transgenic zebrafish expressing either the wild-type or a phosphorylation-resistant form of CagA exhibited significantly increased rates of intestinal epithelial cell proliferation and showed significant upregulation of the Wnt target genes cyclinD1, axin2 and the zebrafish c-myc ortholog myca. Coexpression of CagA with a loss-of-function allele encoding the β-catenin destruction complex protein Axin1 resulted in a further increase in intestinal proliferation. Coexpression of CagA with a null allele of the key β-catenin transcriptional cofactor Tcf4 restored intestinal proliferation to wild-type levels. These results provide in vivo evidence of Wnt pathway activation by CagA downstream of or in parallel to the β-catenin destruction complex and upstream of Tcf4. Long-term transgenic expression of wild-type CagA, but not the phosphorylation-resistant form, resulted in significant hyperplasia of the adult intestinal epithelium. We further utilized this model to demonstrate that oncogenic cooperation between CagA and a loss-of-function allele of p53 is sufficient to induce high rates of intestinal small cell carcinoma and adenocarcinoma, establishing the utility of our transgenic zebrafish model in the study of CagA-associated gastrointestinal cancers.
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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.