Abstract
Helicobacter pylori was reported to be an important risk factor for the carcinogenesis of gastric cancer. Here, we used a proteomic approach to find differentially expressed proteins between the normal and tumor tissue of gastric cancer patients infected with H. pylori. In our results, we found annexin A4 was over-expressed in patients infected with H. pylori and was found in tumor cells, and over-expressed in gastric cancer SCM-1 cells after H. pylori infection. Ca2+ can be induced by H. pylori and interact with annexin A4 Ca2+ binding site to block the calmodulin-activated chloride conductance activation; therefore, it produces a new environment that benefits the malignant existence of H. pylori and raises the risk for gastric cancer. We also found interleuken-8 (IL-8) expression levels were increased in H. pylori infected SCM-1 cells. Combined with previous reports and our results, we summarize that the over-expression of annexin A4 in SCM-1 cells with H. pylori infection may subsequently induce IL-8 which can further cause tumor angiogenesis. In this paper, we show that annexin A4 is a potential novel molecular marker for gastric cancer with H. pylori infection, and our results may provide a new insight in the development of new anti-cancer drugs.
Original language | English (US) |
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Pages (from-to) | 619-634 |
Number of pages | 16 |
Journal | Proteomics - Clinical Applications |
Volume | 2 |
Issue number | 4 |
DOIs | |
State | Published - Apr 2008 |
Externally published | Yes |
Keywords
- 2-DE
- Annexin A4
- Gastric cancer
- Helicobactor pylori
- Structure modeling
ASJC Scopus subject areas
- Clinical Biochemistry