ArticlePLoS pathogens2012
Transgenic expression of the Helicobacter pylori virulence factor CagA promotes apoptosis or tumorigenesis through JNK activation in Drosophila.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Remodeling of the gastric environment inmSystems · 2024Article
- A review of signal pathway induced by virulent protein CagA ofFrontiers in cellular and infection microbiology · 2023Review
- Helicobacter pylori Infection, Its Laboratory Diagnosis, and Antimicrobial Resistance: a Perspective of Clinical Relevance.Clinical microbiology reviews · 2022Review
- Biomarker Characterization and Prediction of Virulence and Antibiotic Resistance fromBiomolecules · 2022Review
- Inter-Species Rescue of Mutant Phenotype-The Standard for Genetic Analysis of Human Genetic Disorders inInternational journal of molecular sciences · 2022Review
- Review
- Review
- The Helicobacter pylori Cag Type IV Secretion System.Trends in microbiology · 2020Review
- Bacterial CagA protein compromises tumor suppressor mechanisms in gastric epithelial cells.The Journal of clinical investigation · 2020Article
- Current understanding and management ofF1000Research · 2018Review
- The bacterial virulence factor CagA induces microbial dysbiosis that contributes to excessive epithelial cell proliferation in the Drosophila gut.PLoS pathogens · 2017Article
- Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels.Scientific reports · 2017Article
- Article
- Article
- Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis.World journal of gastroenterology · 2015Review
- Microbial Regulation of p53 Tumor Suppressor.PLoS pathogens · 2015Review
- Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways.Cell communication and signaling : CCS · 2015Review
- Helicobacter pylori CagA Suppresses Apoptosis through Activation of AKT in a Nontransformed Epithelial Cell Model of Glandular Acini Formation.BioMed research international · 2015Article
- Use of larvae of the wax moth Galleria mellonella as an in vivo model to study the virulence of Helicobacter pylori.BMC microbiology · 2014Article
- Interactions between pork consumption, CagA status and IL-1B-31 genotypes in gastric cancer.World journal of gastroenterology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Gastric cancer development is strongly correlated with infection by Helicobacter pylori possessing the effector protein CagA. Using a transgenic Drosophila melanogaster model, we show that CagA expression in the simple model epithelium of the larval wing imaginal disc causes dramatic tissue perturbations and apoptosis when CagA-expressing and non-expressing cells are juxtaposed. This cell death phenotype occurs through activation of JNK signaling and is enhanced by loss of the neoplastic tumor suppressors in CagA-expressing cells or loss of the TNF homolog Eiger in wild type neighboring cells. We further explored the effects of CagA-mediated JNK pathway activation on an epithelium in the context of oncogenic Ras activation, using a Drosophila model of metastasis. In this model, CagA expression in epithelial cells enhances the growth and invasion of tumors in a JNK-dependent manner. These data suggest a potential role for CagA-mediated JNK pathway activation in promoting gastric cancer progression.
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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.