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Gastrokine 1 inhibits the carcinogenic potentials of Helicobacter pylori CagA.
- Source :
-
Carcinogenesis [Carcinogenesis] 2014 Nov; Vol. 35 (11), pp. 2619-29. Date of Electronic Publication: 2014 Sep 19. - Publication Year :
- 2014
-
Abstract
- Helicobacter pylori CagA directly injected by the bacterium into epithelial cells via a type IV secretion system, leads to cellular changes such as morphology, apoptosis, proliferation and cell motility, and stimulates gastric carcinogenesis. We investigated the effects of cytotoxin-associated gene A (CagA) and gastrokine 1 (GKN1) on cell proliferation, apoptosis, reactive oxygen species (ROS) production, epithelial-mesenchymal transition (EMT) and cell migration in CagA- or GKN1-transfected gastric epithelial cells and mucosal tissues from humans and mice infected with H.pylori. On the molecular level, H.pylori CagA induced increased cell proliferation, ROS production, antiapoptotic activity, cell migration and invasion. Moreover, CagA induced activation of NF-κB and PI3K/Akt signaling pathways and EMT-related proteins. In addition, H.pylori CagA reduced GKN1 gene copy number and expression in gastric cells and mucosal tissues of humans and mice. However, GKN1 overexpression successfully suppressed the carcinogenic effects of CagA through binding to CagA. These results suggest that GKN1 might be a target to inhibit the effects from H.pylori CagA.<br /> (© The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)
- Subjects :
- Animals
Antigens, Bacterial genetics
Apoptosis genetics
Bacterial Proteins antagonists & inhibitors
Bacterial Proteins genetics
Cell Line, Tumor
Cell Movement genetics
Cell Proliferation genetics
Epithelial Cells microbiology
Epithelial Cells pathology
Helicobacter pylori genetics
Humans
Mice
Reactive Oxygen Species
Stomach Neoplasms microbiology
Stomach Neoplasms pathology
Epithelial-Mesenchymal Transition
Helicobacter pylori pathogenicity
Peptide Hormones genetics
Stomach Neoplasms genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1460-2180
- Volume :
- 35
- Issue :
- 11
- Database :
- MEDLINE
- Journal :
- Carcinogenesis
- Publication Type :
- Academic Journal
- Accession number :
- 25239641
- Full Text :
- https://doi.org/10.1093/carcin/bgu199