Helicobacter pylori-induced aberrant methylation of ID4 mediated by DNMT3B drives gastric cancer progression via DEC1-SHH signaling pathway.

ABSTRACT: Helicobacter pylori (H. pylori) infection mediates activation of oncogenes and inhibition of tumor suppressor genes through aberrant DNA methylation, which is the predominant risk factor for gastric tumorigenesis. Here, by integrating transcriptome and epigenetic multi-omics analyses of gastric tissues and mouse models, we identified that inhibitor of differentiation 4 (ID4) was downregulated in H. pylori-infected gastric tissues and associated with prognosis of gastric cancer (GC). H. pylori infection remarkably increased the methylation level of the ID4 promoter region in the GC patients and mouse models. ID4 served as a tumor suppressor gene in GC and was required for H. pylori-mediated tumorigenic activities in vitro cellular and in vivo tumor-bearing mouse models. Moreover, H. pylori

SUBMITTER: Luan M 

PROVIDER: S-EPMC12504463 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature