Journal
ANTICANCER RESEARCH
Volume 42, Issue 1, Pages 531-546Publisher
INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.15511
Keywords
Helicobacter pylori; human gastric adenocarcinoma AGS cells; heat shock proteins family (HSP); iTRAQ proteomic; Ingenuity pathway analysis (IPA)
Categories
Funding
- China Medical University Hospital [DMR-107-134]
- Ministry of Science and Technology, Taiwan [105-2320-B039-039]
- Taipei Veterans General hospital [V110B-038]
- Yen Tjing Ling Medical Foundation [CI-110-6]
- Melissa Lee Cancer Foundation [MLCF-V110-11001]
Ask authors/readers for more resources
This study investigated the expression levels of heat shock proteins in Helicobacter pylori-infected gastric adenocarcinoma cells and found that H. pylori decreases the expression of heat shock proteins in these cells through the regulation of EIF2 and BAG2 signaling pathways.
Background/Aim: Helicobacter pylori, a gramnegative bacterium, causes chronic stomach diseases in humans. Heat shock proteins (HSPs) are involved in cell integrity, cell growth, and gastric mucosa colonization by H. pylori. This study aimed to investigate HSP expression levels in H. pylori-infected gastric adenocarcinoma AGS cells. Materials and Methods: We determined protein expression levels using iTRAQ proteomics analysis. We analyzed the possible network interactions for H. pylori targets in AGS cells using the Ingenuity Pathway Analysis (IPA) software. Results: H. pylori-infected AGS cells potentially targeted EIF2 and BAG2 signaling pathways to regulate cell physiology. In addition, after 3, 6, and 12 h of infection, western blotting revealed significantly decreased HSP70 and HSP105 expression. Conclusion: H. pylori decreases HSPs in AGS gastric adenocarcinoma cells, and this is associated with the regulation of EIF2 and BAG2 signaling pathways.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available