2014
DOI: 10.1038/ncomms5423
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Helicobacter pylori CagA promotes Snail-mediated epithelial–mesenchymal transition by reducing GSK-3 activity

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Cited by 90 publications
(70 citation statements)
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“…We proposed that the activity of secreted HtrA is maybe the initial step in a signaling cascade, followed by CagA and probably others, that triggers EMT in gastric epithelial cells. Translocated CagA can then deregulate cell polarity and scattering, by various pathways including the interaction with partioning kinase Par1b changing cell polarity [66] and by stabilizing Snail, a transcriptional repressor of E-cadherin expression [67]. Taken together, these data provide for the first time genetic evidence that HtrA is a major novel virulence factor of H. pylori , controlling multiple pathogenic activities of this important microbe.…”
Section: Discussionmentioning
confidence: 99%
“…We proposed that the activity of secreted HtrA is maybe the initial step in a signaling cascade, followed by CagA and probably others, that triggers EMT in gastric epithelial cells. Translocated CagA can then deregulate cell polarity and scattering, by various pathways including the interaction with partioning kinase Par1b changing cell polarity [66] and by stabilizing Snail, a transcriptional repressor of E-cadherin expression [67]. Taken together, these data provide for the first time genetic evidence that HtrA is a major novel virulence factor of H. pylori , controlling multiple pathogenic activities of this important microbe.…”
Section: Discussionmentioning
confidence: 99%
“…Through the complex formation, CagA sequesters GSK-3β to the insoluble fraction and thus potentiates Wnt activation by inhibiting the GSK-3β kinase activity. 98) …”
Section: Epiya-independent Caga Functionsmentioning
confidence: 99%
“…94,96) CagA also promotes EMT by inhibiting GSK-3β, which results in stabilization of Snail, a transcriptional repressor of E-cadherin. 98) Mechanistically, CagA-mediated deregulation of Wnt signaling in gastric epithelial cells induces ectopic expression of the Caudal-related homeobox transcription factor Cdx1, which in turn transactivates reprogramming factors such as Sal-like protein 4 (SALL4) and Krüppel-like factor 5 (KLF5) to confer a stem-cell property in gastric epithelial cells. This CagA-mediated cell-fate reprogramming may underlie intestinal metaplasia, abnormal transdifferentiation of gastric epithelial cells to intestinal-like cells, that occurs in gastric mucosa that has been chronically infected with cagA -positive H. pylori .…”
Section: Caga Reprogramming and Genetic Instabilitymentioning
confidence: 99%
“…Cytotoxin-associated gene A (CagA) is an onco-protein and a major virulence factor of H. pylori . Recent article regarding EMT on gastric cancer suggests that CagA of H. pylori plays a decisive role that triggers a EMT through several transcription factors activation 18. Up to recently, it was speculated that miRNA- related EMT might be regulated by hsa-miR-335, hsa-miR-21, hsa-miR-31, hsa-miR-205, and hsa-miR-10b 19.…”
Section: Discussionmentioning
confidence: 99%