From infection to invasion: The role of deleted in malignant brain tumors 1 in Helicobacter pylori-driven gastric cancer.

Gastric cancer (GC) remains a major health challenge worldwide, with Helicobacter pylori (H. pylori) infection playing a key role in its development. H. pylori creates a mutagenic environment in the stomach by causing chronic inflammation, oxidative DNA damage, inducing DNA double-strand breaks, and disrupting DNA repair mechanisms and cell cycle checkpoints. Cytotoxin-associated gene A is the main carcinogenic component of H. pylori and interacts with signaling pathways to promote carcinogenesis. Deleted in malignant brain tumors 1 (DMBT1), a potential tumor suppressor gene, shows variable expression patterns in GC. DMBT1 is frequently downregulated in well-differentiated gastric adenocarcinomas but upregulated in other GC types. The correlation between DMBT1 expression and H. pylori infection is important, as maintained DMBT1 expression in precancerous states may protect against gastric carcinogenesis, while its downregulation may facilitate tumor progression. DMBT1 functions as a pattern recognition receptor that binds to H. pylori and other pathogens and modulates inflammatory and immune responses. H. pylori colonization of gastric mucosa can induce an inflammatory microenvironment, which influences tumor suppressor gene expression, including DMBT1. Understanding the interactions between DMBT1 and H. pylori may reveal new therapeutic targets and preventive strategies for H. pylori-associated gastric disease.