Helicobacter pylori eradication down-regulates cellular inhibitor of apoptosis protein 2 in gastric carcinogenesis

Abstract

Background: To evaluate the expression of cellular inhibitor of apoptosis protein 2 (cIAP2) during gastric carcinogenesis after Helicobacter pylori (HP) infection and after HP eradication Methods: We divided non-cancer patients into 4 groups according to the status of HP infection and atrophic gastritis (AG)/intestinal metaplasia (IM)

we compared cIAP2 mRNA expression among these 4 groups and patients with HP-positive early gastric cancer (EGC) by real-time PCR. We evaluated the expression of cIAP2 mRNA/protein by real-time PCR/immunohistochemistry, and the degree of apoptosis by TUNEL assay before and 12 months after endoscopic submucosal dissection (ESD) in HP-positive EGC patients irrespective of whether they received eradication therapy. Results: The expression of cIAP2 mRNA was significantly higher in groups with HP(+) and AG/IM(+) and HP-positive EGC than in the control, HP(+) and AG/IM(-) groups (p < 0.005). In the HP eradication group, the expression of cIAP2 mRNA/protein significantly decreased (p = 0.006) and apoptosis increased at the 12-month follow-up after ESD. In the HP non-eradication group, the aforementioned changes were not found at the same follow-up period. Conclusion: The expression of cIAP2 increased during gastric carcinogenesis after HP infection

HP eradication in the patients who underwent ESD for EGC reversed the over-expression of cIAP2 and suppressed cell apoptosis.