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Helicobacter pylori CagA protein targets the c-Met receptor and enhances the motogenic response
Open accessAbstract
Infection with the human microbial pathogen Helicobacter pylori is assumed to lead to invasive gastric cancer. We find that H. pylori activates the hepatocyte growth factor/scatter factor receptor c-Met, which is involved in invasive growth of tumor cells. The H. pylori effector protein CagA intracellularly targets the c-Met receptor and promotes cellular processes leading to a forceful motogenic response. CagA could represent a bacterial adaptor protein that associates with phospholipase Cγ but not Grb2-associated binder 1 or growth factor receptor–bound protein 2. The H. pylori–induced motogenic response is suppressed and blocked by the inhibition of PLCγ and of MAPK, respectively. Thus, upon translocation, CagA modulates cellular functions by deregulating c-Met receptor signaling. The activation of the motogenic response in H. pylori–infected epithelial cells suggests that CagA could be involved in tumor progression.
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“CagA binds to and activates c-Met, stimulating epithelial cell motility and invasiveness, processes that are precursors to carcinogenesis [32].”
From Candida albicans stimulates formation of a multi-receptor complex that mediates epithelial cell invasion during oropharyngeal infection (2023) · cites this paper as [32]
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“Helicobacter pylori activates c-Met by injecting cytotoxin-associated gene A (CagA) into gastric epithelial cells via the type IV secretion system.”
From Candida albicans stimulates formation of a multi-receptor complex that mediates epithelial cell invasion during oropharyngeal infection (2023) · cites this paper as [32]
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Metadata
- Authors
- Churin, Y., Al-Ghoul, L., Kepp, O., Meyer, T. F., Birchmeier, W., & Naumann, M.
- Affiliations
- Max Planck Institute for Infection Biology (DE)
- Otto-von-Guericke-Universität Magdeburg (DE)
- Max Delbrück Center (DE)
- Max Planck Society (DE)
- Corresponding author
- Naumann, Michael
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2003-04-28
- Volume
- 161
- Issue
- 2
- Pages
- 249-255
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2172921
- OpenAlex
- W1991444764
- Cited by
- 354
- References
- 31
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 9 · 2022: 9 · 2021: 6 · 2020: 11 · 2019: 15 · 2018: 8 · 2017: 25 · 2016: 16 · 2015: 10 · 2014: 17 · 2013: 14 · 2012: 14
- FWCI
- 26.28
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (acceptedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Health Sciences › Medicine › Gastroenterology › Helicobacter pylori-related gastroenterology studies
- Health Sciences › Medicine › Oncology › Gastric Cancer Management and Outcomes
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- Helicobacter pylori, CagA, c-Met, hepatocyte growth factor, bacterial effector proteins, cell motility, phospholipase C-gamma, MAPK signaling, gastric cancer, tumor progression, epithelial cells, receptor translocation
- MeSH terms
- Antigens, Bacterial, Bacterial Proteins, Carcinoma, Cell Division, Cell Transformation, Neoplastic, Enzyme Inhibitors, Humans, Type C Phospholipases, Phosphoproteins, Proteins, Stomach Neoplasms, Tumor Cells, Cultured, Signal Transduction, Helicobacter pylori, Helicobacter Infections, Hepatocyte Growth Factor, Proto-Oncogene Proteins c-met, Mitogen-Activated Protein Kinase 1, Protein Transport, Adaptor Proteins, Signal Transducing, GRB2 Adaptor Protein, Phospholipase C gamma
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