ArticleProceedings of the National Academy of Sciences of the United States of America2005
Helicobacter pylori CagA induces a transition from polarized to invasive phenotypes in MDCK cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
134 citing papers in PubMed, 1 synthesis or guideline pooled it, 260 citations in OpenAlex.
- Association of CagA EPIYA-D or EPIYA-C phosphorylation sites with peptic ulcer and gastric cancer risks: A meta-analysis.Medicine · 2017Pooled it
- The "Hit-and-Run" legacy: epigenetic locking and the survival switch in H. pylori-associated gastric cancer.Cell death discovery · 2026Review
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- Microbiome modulation of tumorigenesis and immune responses.Journal of biomedical science · 2026Review
- A Narrative Review on Unravelling Bacterial-Mediated Carcinogenesis and Possible Alternative Treatment Strategies.BioMed research international · 2026Review
- Pathogenicity ofWorld journal of clinical oncology · 2025Review
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- The Toxoplasma secreted effector TgWIP modulates dendritic cell motility by activating host tyrosine phosphatases Shp1 and Shp2.Cellular and molecular life sciences : CMLS · 2024Article
- The Toxoplasma secreted effector TgWIP modulates dendritic cell motility by activating host tyrosine phosphatases Shp1 and Shp2.Research square · 2024Article
- Anti-inflammatory effects of eupatilin on Helicobacter pylori CagA-induced gastric inflammation.PloS one · 2024Article
- IL-8 Secreted by Gastric Epithelial Cells Infected withViruses · 2023Article
- Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development.Current topics in microbiology and immunology · 2023Article
- Unwelcome guests - the role of gland-associatedFrontiers in oncology · 2023Review
- Influence ofWorld journal of clinical oncology · 2022Review
- Cancer-Associated Microbiota: From Mechanisms of Disease Causation to Microbiota-Centric Anti-Cancer Approaches.Biology · 2022Review
- Organoids in recapitulating tumorigenesis driven by risk factors: Current trends and future perspectives.International journal of biological sciences · 2022Review
- Role of the Gastric Microbiome in Gastric Cancer: From Carcinogenesis to Treatment.Frontiers in microbiology · 2021Review
- Review
74 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
CagA is a bacterial effector protein of Helicobacter pylori that is translocated via a type IV secretion system into gastric epithelial cells. We previously described that H. pylori require CagA to disrupt the organization and assembly of apical junctions in polarized epithelial cells. In this study, we provide evidence that CagA expression is not only sufficient to disrupt the apical junctions but also perturbs epithelial differentiation. CagA-expressing cells lose apicobasal polarity and cell-cell adhesion, extend migratory pseudopodia, and degrade basement membranes, acquiring an invasive phenotype. Expression of the CagA C-terminal domain, which contains the tyrosine phosphorylated EPIYA motifs, induces pseudopodial activity but is not sufficient to induce cell migration. Conversely, the N terminus targets CagA to the cell-cell junctions. Neither domain is sufficient to disrupt cell adhesion or cell polarity, but coexpressed in trans, the N terminus determines the localization of both polypeptides. We show that CagA induces a morphogenetic program in polarized Madin-Darby canine kidney cells resembling an epithelial-to-mesenchymal transition. We propose that altered cell-cell and cell matrix interactions may serve as an early event in H. pylori-induced carcinogenesis.
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Identifiers
What OpenQuestion holds
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.