Cited by 354Helicobacter pylori-related gastroenterology studiesGastric Cancer Management and OutcomesGastrointestinal motility and disorders

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Helicobacter pylori CagA protein targets the c-Met receptor and enhances the motogenic response

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Churin, Yuri, Al-Ghoul, Laila, Kepp, Oliver, Meyer, Thomas F., Birchmeier, Walter, Naumann, Michael·2003·The Journal of Cell Biology

DOI 10.1083/jcb.200208039PMC PMC2172921

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Abstract

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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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
ORCID: Churin, Yuri
Kepp, Oliver
Meyer, Thomas F.
Birchmeier, Walter
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
DOI: 10.1083/jcb.200208039
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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Helicobacter pylori CagA protein targets the c-Met receptor and enhances the motogenic response

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