Abstract
The regulatory mechanism of Helicobacter pylori-induced gastric carcinogenesis remains unclear. Autophagy has previously been identified as an effective method of regulating carcinogenesis. In the present study, microRNA (miR)-99b levels increased in H. pylori-infected gastric cancer tissues and the BGC-823 gastric cancer cell line. Overexpression of miR-99b significantly enhanced autophagy, decreased intracellular bacterial loads and blocked cell proliferation. The effect on autophagy was demonstrated to be triggered by mammalian target of rapamycin inhibition. These results indicate that miR-99b expression serves a key role in preventing H. pylori-associated gastric cancer formation and this may provide potential targets for the future treatment of H. pylori-associated diseases.