Helicobacter pylori infection promotes the progression of gastric cancer by regulating the expression of DMBT1.

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. (. ) is the major cause of GC. Managing infections caused by 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 and GC. However, the precise underlying mechanism is unclear.

AIM

To explore the role of DMBT1, as modulated by , in the development, proliferation, and metastasis of GC.

METHODS

Utilizing human GC cells, DMBT1 gene silencing, and treatment, four cell groups (control, , si-DMBT1, and + 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, + si-DMBT1 showed the greatest ability to proliferate, migration, and invasion capabilities, followed by the si-DMBT1, , and control groups. DMBT1 mRNA was found to be the highest in control group, next in si-DMBT1, and + si-DMBT1, while + 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, could enhance GC's proliferation, metastasis and invasion. Our findings revealed a novel connection between infection, inflammation, and GC.