H. pylori SlyD Enhances TPT1 Stability via hnRNPK to Promote OCT1-Mediated CDX2 Transcriptional Activation Triggering Gastric Intestinal Metaplasia
Gastric intestinal metaplasia (GIM) is an important precancerous lesion in intestinal-type gastric cancer, with persistent Helicobacter pylori (H. pylori) infection inducing the condition. In a previous study, we identified a new H. pylori virulence factor, SlyD. However, its mode of action between GIM was unknown. Our findings offer clues to reveal the molecular mechanism of H.pylori infection-associated gastric intestinal metaplasia, and provides the mechanism of a novel H. pylori virulence factor SlyD in gastric precancerous disease. Overall design: The H. pylori 26695 was acquired from the American Type Culture Collection (ATCC). A SlyD inactivated mutant strain, where chloramphenicol-resistant fragments replaced slyD fragments (?SlyD), was generated based on H. pylori 26695. AGS cells were exposed to H. pylori 26695 or ?SlyD for 24 hours (MOI = 100). Total RNA was extracted for RNA sequencing. RNA sequencing was used to screen for differentially expressed genes associated with H. pylori SlyD infection.