Abstract: Objective To explore the molecular involvement of Helicobacter pylori in gastric cancer by examining the effects of different H. pylori loads on proliferation，apoptosis and FAF1 mRNA expression in gastric cancer cells. Method Human gastric carcinoma HGC-27 cells were co-cultured with different amounts of standard H. pylori strain NCTC11637；multiplicities of infection （MOIs，bacteria/cells） were 0，1，50，100 and 200. H. pylori was identified based on Gram staining and biochemical tests. Cancer cell proliferation was measured using the thiazolyl blue（MTT） assay after 0，12，24，36 and 48 h of co-culture. After 24 h co-culture，apoptosis in the cancer cells was measured using flow cytometry，and FAF1 mRNA expression was quantitated using fluorescent real-time quantitative RT-PCR. Expression of the β-actin gene was used as a reference for normalizing FAF1 mRNA expression levels. Results After 12 h co-culture，cancer cell proliferation at MOI 50 was significantly greater than at MOI 0（P<0.05），whereas proliferation at other MOIs was lower than at MOI 0（P<0.05）. After co-culture for 24，36 and 48 h，cancer cell proliferation at all MOIs was significantly lower than at MOI 0（P<0.05）. After 24 h co-culture，apoptosis levels and relative  FAF1 mRNA expression were similar at MOIs 0，1，and 50 （P＞0.05）. In contrast，apoptosis levels were significantly higher and relative  FAF1 mRNA expression significantly lower at MOIs 100 and 200 than at MOI 0（P<0.05）. Conclusion H. pylori infection can suppress proliferation， promote apoptosis and down-regulate FAF1 mRNA expression in gastric cancer cells-regulation of FAF1 mRNA by H. pylori may lead to gastric cancer.

Key words: Gastric neoplasm, Fas-associated factor 1, Helicobacter pylori, Proliferation；Apoptosis