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

Gastric cancer (GC) remains a major health challenge worldwide, with <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection playing a key role in its development. <i>H. pylori</i> 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 <i>H. pylori</i> and interacts with signaling pathways to promote carcinogenesis. Deleted in malignant brain tumors 1 (<i>DMBT1</i>), a potential tumor suppressor gene, shows variable expression patterns in GC. <i>DMBT1</i> is frequently downregulated in well-differentiated gastric adenocarcinomas but upregulated in other GC types. The correlation between <i>DMBT1</i> expression and <i>H. pylori</i> infection is important, as maintained <i>DMBT1</i> expression in precancerous states may protect against gastric carcinogenesis, while its downregulation may facilitate tumor progression. <i>DMBT1</i> functions as a pattern recognition receptor that binds to <i>H. pylori</i> and other pathogens and modulates inflammatory and immune responses. <i>H. pylori</i> colonization of gastric mucosa can induce an inflammatory microenvironment, which influences tumor suppressor gene expression, including <i>DMBT1</i>. Understanding the interactions between <i>DMBT1</i> and <i>H. pylori</i> may reveal new therapeutic targets and preventive strategies for <i>H. pylori</i>-associated gastric disease.