Abstract: Objective To study the role and mechanism of Helicobacter pylori (HP) infection in regulating the esophageal cancer cell apoptosis through MDM2 / P53 pathway. Methods The resected esophageal cancer tissues were collected and the HP infection, the expression levels of MDM2 and P53 were detected. Esophageal cancer TE-1 cell line was cultured and intervened with HP infection, normal saline ( NS ) or ubiquitin proteasome inhibitor PS341, negative control (NC) siRNA or MDM2 siRNA were transfected into the cells. Cell viability, apoptosis rate, the expression level of MDM2 and P53 and the ubiquitination level of P53 were detected. Results The expression level of MDM2 in the HP positive esophageal cancer tissues was higher than that in the HP negative esophageal cancer tissues, and the expression level of P53 was lower than that in the HP negative esophageal cancer tissues (P < 0. 05). The cell viability, MDM2 expression level and the P53 ubiquitination level in TE-1 cells of the HP group were higher than those in the control group. The apoptosis rate and P53 expression level were lower than those in the control group. The expression level of P53 in TE-1 cells of the PS341 + Hp group was higher than that in the NS + Hp group (P< 0. 05). The cell viability, MDM2 expression level and P53 ubiquitinated level in TE-1 cells of the si-MDM2 + Hp group were lower than those in the si-NC + Hp group, and the apoptosis rate and P53 expression level were higher than those in the si-NC + Hp group (P< 0. 05). Conclusion The inhibitory effect of HP infection on apoptosis of esophageal cancer cells is related to the increasing of the expression level of MDM2 and promotion of the ubiquitination and degradation of P53. 

Key words: esophageal cancer, helicobacter pylori, mdm2, P53, apoptosis, ubiquitination