Helicobacter Pylori Targets the EPHA2 Receptor Tyrosine Kinase in Gastric Cells Modulating Key Cellular Functions.

摘要: Helicobacter pylori, a stomach-colonizing Gram-negative bacterium, is the main etiological factor of various gastroduodenal diseases, including gastric adenocarcinoma. By establishing life-long infection mucosa, H. pylori continuously activates host-signaling pathways, in particular those associated with receptor tyrosine kinases. Using two different epithelial cell lines, we show that targets kinase EPHA2. For long periods time post-infection, induces EPHA2 protein downregulation without affecting its mRNA levels, an effect preceded by activation via phosphorylation. occurs lysosomal degradation pathway and independent virulence factors CagA, VacA, T4SS. small interfering RNA, knockdown affects cell–cell cell–matrix adhesion, invasion, angiogenesis, which are critical cellular processes early lesions carcinogenesis mediated bacteria. This work contributes to unraveling underlying mechanisms pylori–host interactions diseases. Additionally, it raises awareness for potential interference between efficacy cancer therapies targeting receptors kinases, given steady-state levels dynamics some kinases (RTKs) their signaling pathways.