H. pylori infection promotes the proliferation of gastric cancer via CDK1 expression

Abstract

Abstract Backgroud: The pervasiveness of H. pylori infection contributes to numerous gastrointestinal disorders, thus posing a significant challenge for patients and society alike. This research examines the influence of CDK1 in H. pylori infected gastric cancer. Methods: The presence of CDK1 in H. pylori infected GC tissues and cell lines was ascertained through immunohistochemical fluorescence staining, Real-time PCR, and western blot methodologies. Moreover, CDK1 was silenced in GC cells via siRNA, and the mobility and invasive capacity of GC cells with CDK1 suppression were evaluated using Transwell assays. In the end, the levels of inflammation and cell apoptosis were assessed by ELISA and flow cytometry. Results: The findings suggest that CDK1 is elevated in GC tissues and cell lines, showing a significant rise in H. pylori infected GC. Concurrently, H. pylori infection enhances the migratory and invasive potential by modulating CDK1. Further, H. pylori incites a robust cellular inflammatory response and apoptosis by modulating CDK1. Conclusion: The study concludes that H. pylori infection can alter multiple physiological processes in host cells by controlling CDK1, implying that CDK1 could serve as a potential molecular target for combating H. pylori infection.