Abstract
Cellular inhibitor of apoptosis protein 2 (cIAP2) is a member of the IAP family and is over-expressed in most cancer tissues. In this study, we investigated the role cIAP2 in Helicobacter pylori (HP) related gastric carcinogenesis. We measured the expression of cIAP2 at mRNA and protein levels in a panel of gastric cancer cell lines and human gastric cancer tissues by semi-quantitative reverse transcriptase PCR (RT-PCR), quantitative real time PCR (qPCR), immunoblotting, and immunohistochemistry. The effects of cIAP2 down-regulation on gastric cell proliferation and apoptosis were detected by standard WST-1 assay and flow cytometry, respectively. Infection of gastric mucosa by HP enhances the expression of cIAP2 in mouse gastric tissues. Over 70% of human gastric cancer tissues express higher amount of cIAP2. Well-differentiated gastric cancer cells express more cIAP2 than moderately- and poorly-differentiated gastric cancer cells. Knocking down of cIAP2 in SGC-7901 cells results in a 30% decrease in cell proliferation, a 20% increase in apoptosis and delayed migration. Thus, cIAP2 may play an important role in HP-induced gastric carcinogenesis, and it may serve as a potential target for gastric cancer therapy.
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