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The control of H. pylori-mediated gastric cancer development and progression through YAP/TAZ signal regulation

GSE275727 Homo sapiens Expression profiling by high throughput sequencing 9 samples Submitted 2024/10/28 Platform GPL21697
Summary
Helicobacter pylori(H. pylori), a gastrointestinal pathogen, is known to increase the risk of gastric cancer by activating chronic pro-inflammatory signaling pathways in epithelial cells. Cytotoxin-related protein A (CagA) is known to play an important role in gastric cancer development. CagA has been reported to induce tumors by inducing overexpression of YAP/TAZ, a component of Hippo signaling, and dysregulation of the pathway, thereby promoting cell proliferation and resistance to apoptosis. However, the role of H.pylori-mediated YAP/TAZ has not yet been fully investigated. Our study aimed to investigate the role of YAP/TAZ in H.pylori-mediated Hippo pathway dysregulation in gastric carcinogenesis using H.pylori-infected gastric cancer cell lines, knockout mice, and patient-derived organoids. CagA-mediated YAP overexpression in gastric epithelial cells induced intestinal epithelial metaplasia and induced intracellular rearrangement of the binding protein ZO1, thereby conferring cell motility.
Published in
Yes-Associated Protein Drives Helicobacter pylori-Induced Metaplastic Changes in Gastric Epithelium
Yu BM, Lee SD, Hwang BR et al. · Cellular and molecular gastroenterology and hepatology 2026 · PMID 42173319 · doi:10.1016/j.jcmgh.2026.101814
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Also filed as BioProject PRJNA1152793 and SRA study SRP528810. Searching any of these in the dataset finder brings you back here.

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