Helicobacter pylori infection induces STAT3/MYBL2/NF-κB axis to promote gastric cancer progression.

Infection with Helicobacter pylori (H. pylori) represents a significant risk factor for the development of gastric cancer (GC). The oncogenic functions of MYBL2 have been reported in several malignancies, for which little research has focused on its effect on H. pylori-induced GC progression. We analyzed the expression and clinical relevance of MYBL2 in GC. H. pylori infection was induced in vitro and in vivo. The effects of MYBL2 on cellular functions were assessed, and tumor growth was evaluated in nude mice injected with genetically altered GC cells. We found H. pylori infection significantly increased MYBL2 expression. Downregulation of MYBL2 inhibited H. pylori-induced cell proliferation and migration. MYBL2 contributed to the growth of subcutaneous xenograft tumors. In conclusion, H. pylori infection upregulated MYBL2 expression by activating STAT3, and MYBL2 was found to be an upstream regulator of NF-κB activation in GC cells. In conclusion, our findings indicate that the H. pylori/STAT3/MYBL2/NF-κB axis plays a critical role in the regulation of GC.