ArticleThe Journal of experimental medicine2010
Conversion of Helicobacter pylori CagA from senescence inducer to oncogenic driver through polarity-dependent regulation of p21.
Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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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.
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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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Roles of microRNAs and exosomes in Helicobacter pylori associated gastric cancer.Molecular biology reports · 2023Pooled it
- The cellular stress sensor HSPB1 regulates the membrane localization of amino acid transporter SLC7A5 in breast cancer.The Journal of biological chemistry · 2026Article
- Helicobacter pylori, microbiota and gastric cancer - principles of microorganism-driven carcinogenesis.Nature reviews. Gastroenterology & hepatology · 2025Review
- Association ofFrontiers in medicine · 2025Review
- Amino acid deletions at positions 893 and 894 of cytotoxin-associated gene A protein affectWorld journal of gastroenterology · 2024Article
- Polarity protein SCRIB interacts with SLC3A2 to regulate proliferation and tamoxifen resistance in ER+ breast cancer.Communications biology · 2022Article
- Mouse Gastric Epithelial Cells Resist CagA Delivery by theInternational journal of molecular sciences · 2022Article
- TheInternational journal of molecular sciences · 2022Article
- Organoids in recapitulating tumorigenesis driven by risk factors: Current trends and future perspectives.International journal of biological sciences · 2022Review
- Senescence: A Novel Driver of Helicobacter pylori-Induced Gastric Atrophy.Cellular and molecular gastroenterology and hepatology · 2021Article
- The gut microbiome and frailty.Translational research : the journal of laboratory and clinical medicine · 2020Review
- Detection of Novel Amino Acid Polymorphisms in the East Asian CagA of Helicobacter Pylori with Full Sequencing Data.The Kobe journal of medical sciences · 2020Article
- CagA-ASPP2 complex mediates loss of cell polarity and favorsProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Molecular anatomy and pathogenic actions of Helicobacter pylori CagA that underpin gastric carcinogenesis.Cellular & molecular immunology · 2020Review
- Review
- Article
- Article
- The Post-amyloid Era in Alzheimer's Disease: Trust Your Gut Feeling.Frontiers in aging neuroscience · 2019Review
- Review
- Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Helicobacter pylori CagA bacterial oncoprotein plays a critical role in gastric carcinogenesis. Upon delivery into epithelial cells, CagA causes loss of polarity and activates aberrant Erk signaling. We show that CagA-induced Erk activation results in senescence and mitogenesis in nonpolarized and polarized epithelial cells, respectively. In nonpolarized epithelial cells, Erk activation results in oncogenic stress, up-regulation of the p21(Waf1/Cip1) cyclin-dependent kinase inhibitor, and induction of senescence. In polarized epithelial cells, CagA-driven Erk signals prevent p21(Waf1/Cip1) expression by activating a guanine nucleotide exchange factor-H1-RhoA-RhoA-associated kinase-c-Myc pathway. The microRNAs miR-17 and miR-20a, induced by c-Myc, are needed to suppress p21(Waf1/Cip1) expression. CagA also drives an epithelial-mesenchymal transition in polarized epithelial cells. These findings suggest that CagA exploits a polarity-signaling pathway to induce oncogenesis.
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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.