Cited by 155Helicobacter pylori-related gastroenterology studiesCytokine Signaling Pathways and InteractionsGastric Cancer Management and Outcomes

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Helicobacter pylori Cytotoxin-Associated Gene A Activates the Signal Transducer and Activator of Transcription 3 Pathway In vitro and In vivo

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Bronte-Tinkew, Dana M., Terebiznik, Mauricio, Franco, Aime, Ang, Michelle, Ahn, Diane, Mimuro, Hitomi, Sasakawa, Chihiro, Ropeleski, Mark J., Peek, Richard M., Jones, Nicola L.·2009·Cancer Research

DOI 10.1158/0008-5472.can-08-1191PMC PMC3418672

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Abstract

Persistent infection with Helicobacter pylori confers an increased risk for the development of gastric cancer. However, the exact mechanisms whereby this bacterium causes carcinogenesis have not been completely elucidated. Recent evidence indicates that aberrant activation of the signal transducers and activators of transcription 3 (STAT3) signaling pathway may play a role in gastric carcinogenesis. Therefore, we hypothesized that H. pylori infection modulates STAT3 signaling, favoring gastric cancer development. In epithelial cells infected with H. pylori, STAT3 was activated, as assessed by immunoblotting for phosphorylated STAT3, immunofluorescence of translocated STAT3, fluorescence recovery after photobleaching, and luciferase activation in transfected cells. Activation was dependent on translocation but not phosphorylation of cytotoxin-associated gene A (CagA) in host cells. Activation seemed to be receptor-mediated because preincubation of cells with the interleukin-6 (IL-6) receptor superantagonist sant7 or inhibition of gp130 by a monoclonal antibody prevented H. pylori–mediated STAT3 activation. However, activation was not related to autocrine activation by IL-6 or IL-11. CagA+ wild-type H. pylori, but not the noncarcinogenic cagA− mutant, activated STAT3 in gastric epithelial cells in vivo in the gerbil model of H. pylori–mediated gastric carcinogenesis. Collectively, these results indicate that H. pylori CagA activates the STAT3 signaling pathway in vitro and in vivo, providing a potential mechanism by which chronic H. pylori infection promotes the development of gastric cancer. [Cancer Res 2009;69(2):632–9]

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Self-citation
H. pylori induces the expression of Hath1 in gastric epithelial cells via interleukin‐8/STAT3 phosphorylation while suppressing Hes1
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Authors: Bronte-Tinkew, D. M., Terebiznik, M., Franco, A., Ang, M., Ahn, D., Mimuro, H., Sasakawa, C., Ropeleski, M. J., Peek, R. M., & Jones, N. L.
Affiliations: University of Toronto (CA)
Vanderbilt University (US)
Institute of Medical Science, The University of Tokyo (JP)
Queen's University (CA)
ORCID: Terebiznik, Mauricio
Franco, Aime
Mimuro, Hitomi
Sasakawa, Chihiro
Peek, Richard M.
Jones, Nicola L.
Venue: Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2009-01-15
Volume: 69
Issue: 2
Pages: 632-639
ISSN: 0008-5472 (ISSN-L)
1538-7445
DOI: 10.1158/0008-5472.can-08-1191
PMC: PMC3418672
OpenAlex: W2117113786
Cited by: 154
References: 33
Citations by year: 2026: 7 · 2025: 9 · 2024: 8 · 2023: 14 · 2022: 7 · 2021: 6 · 2020: 10 · 2019: 5 · 2018: 6 · 2017: 8 · 2016: 11 · 2015: 8 · 2014: 11 · 2013: 13 · 2012: 13
FWCI: 10.48
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Cancer Research (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (R29CA077955, CA-77955, R01CA077955)
National Institute of Diabetes and Digestive and Kidney Diseases (DK-73902, R01DK058587, DK-58587, R01DK073902)
Topics: Health Sciences › Medicine › Gastroenterology › Helicobacter pylori-related gastroenterology studies
Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
Health Sciences › Medicine › Oncology › Gastric Cancer Management and Outcomes
Keywords: Helicobacter pylori, CagA, cytotoxin-associated gene A, STAT3 signaling, gastric carcinogenesis, gp130, IL-6 receptor, interleukin-11, chronic infection, gastric epithelial cells, gerbil model
MeSH terms: Adenocarcinoma, Animals, Antigens, Bacterial, Bacterial Proteins, Cell Nucleus, Gerbillinae, HeLa Cells, Humans, Male, Phosphorylation, Stomach Neoplasms, Transcription, Genetic, Tyrosine, Helicobacter pylori, Helicobacter Infections, Receptors, Interleukin-6, Cell Line, Tumor, STAT3 Transcription Factor, Cytokine Receptor gp130

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Helicobacter pylori Cytotoxin-Associated Gene A Activates the Signal Transducer and Activator of Transcription 3 Pathway In vitro and In vivo

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