Helicobacter pylori-induced alteration of epithelial cell signaling and polarity: A possible mechanism of gastric carcinoma etiology and disparity

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dc.contributor.authorOsman, M.A.
dc.contributor.authorBloom, G.S.
dc.contributor.authorTagoe, E.A.
dc.date.accessioned2018-12-12T15:50:20Z
dc.date.available2018-12-12T15:50:20Z
dc.date.issued2013-07
dc.description.abstractGastric cancer, a disease of disparity associated with Helicobacter pylori (H. pylori) infection, is the world's second leading cause of cancer deaths. The pathogen H. pylori target the epithelial adhesion receptors, E-cadherin, and β1-integrin, to modulate the host cytoskeleton via disruption of the epithelial cell polarity necessary for maintaining the infection, but how this leads to the development of the carcinoma is widely unclear. While Rho family GTPases' signaling to the cytoskeleton and these receptors is required for initiating and maintaining the infection, the responsible effectors, and how they might influence the etiology of the carcinomas are currently unknown. Here we discuss the potential role of the Cdc42-IQGAP1 axis, a negative regulator of the tumor suppressors E-cadherin and β1-integrin, as a potential driver of H. pylori-induced gastric carcinoma and propose avenues for addressing its disparity. Chronic dysfunction of the IQGAP1-signaling pathway, resulting from H. pylori-induced disruption of cell polarity, can explain the pathogenesis of the carcinoma, at least, in subsets of infected population, and thus could provide a potential means for personalized medicine. © 2013 Wiley Periodicals, Inc.en_US
dc.identifier.otherhttps://doi.org/10.1002/cm.21114
dc.identifier.otherVolume 70, Issue 7, Pages 349-359
dc.identifier.urihttp://ugspace.ug.edu.gh/handle/123456789/26373
dc.language.isoenen_US
dc.publisherCytoskeletonen_US
dc.subjectAkten_US
dc.subjectCdc42en_US
dc.subjectErk1/2en_US
dc.subjectGastric canceren_US
dc.subjectH. pylorien_US
dc.subjectIQGAPen_US
dc.subjectMTORen_US
dc.titleHelicobacter pylori-induced alteration of epithelial cell signaling and polarity: A possible mechanism of gastric carcinoma etiology and disparityen_US
dc.typeOtheren_US

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