Abstract
BACKGROUND: Each year, more than a million people are diagnosed with gastric cancer (GC) worldwide, and the incidence of this disease is projected to increase. Helicobacter pylori (H. pylori) is the major cause of GC. Managing infections caused by H. pylori and investigating their contribution to GC carcinogenesis are crucial for advancing diagnosis and treatment. Deleted in malignant brain tumors 1 (DMBT1) is associated with the development of H. pylori and GC. However, the precise underlying mechanism is unclear. AIM: To explore the role of DMBT1, as modulated by H. pylori, in the development, proliferation, and metastasis of GC. METHODS: Utilizing human GC cells, DMBT1 gene silencing, and H. pylori treatment, four cell groups (control, H. pylori, si-DMBT1, and H. pylori + si-DMBT1) were subjected to cell counting kit-8, scratch, and Transwell assays. The DMBT1 expression was assessed by quantitative real-time polymerase chain reaction and Western blot. RESULTS: In cellular tests, H. pylori + si-DMBT1 showed the greatest ability to proliferate, migration, and invasion capabilities, followed by the si-DMBT1, H. pylori, and control groups. DMBT1 mRNA was found to be the highest in control group, next in si-DMBT1, H. pylori and H. pylori + si-DMBT1, while H. pylori + si-DMBT1 showed the least expression. The results the Western blot assay showed a consistent trend of decreasing DMBT1 protein and mRNA levels. CONCLUSION: Through inhibition of DMBT1, H. pylori could enhance GC's proliferation, metastasis and invasion. Our findings revealed a novel connection between H. pylori infection, inflammation, and GC.