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dc.contributor.advisorMeuillet, Emmanuelle J.en_US
dc.contributor.authorComer, Shawna Beth
dc.creatorComer, Shawna Bethen_US
dc.date.accessioned2011-12-05T14:13:22Z
dc.date.available2011-12-05T14:13:22Z
dc.date.issued2007en_US
dc.identifier.urihttp://hdl.handle.net/10150/193312
dc.description.abstractResearch has identified a linear relationship between saturated fat intake and colon cancer, and has demonstrated that high fat diets enhance tumorigenesis through elevation of secondary bile acids such as deoxycholic acid (DCA). We and others have shown that DCA can manipulate cell adhesion by decreasing expression of E-cadherin and increasing expression of beta-catenin. We have also shown that DCA significantly reduces EphB2 expression, which regulates cell positioning and segregation. Importantly, vitamin D can reinstate membranous E-cadherin/beta-catenin interactions and increase E-cadherin expression. In the present study, we sought to analyze the effects of DCA and vitamin D (cholecalciferol) treatment on EphB2 in colorectal cancer cells. Pre-treatment with cholecalciferol restored EphB2 expression in a dose-dependent manner, even with combined DCA treatment. This observation may be EGFR-dependent, suggesting that cholecalciferol may antagonize the effects of DCA. Taken together, these results suggest that cholecalciferol may represent an adjuvant therapy for colorectal cancer patients.
dc.language.isoENen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.subjectEphB2en_US
dc.subjectcolorectal canceren_US
dc.subjectcell adhesionen_US
dc.subjectE-cadherinen_US
dc.subjectvitamin Den_US
dc.subjectbile acidsen_US
dc.titleCholecalciferol Protects Against Deoxycholic Acid-Induced Loss of EphB2 in Human Colorectal Cancer Cellsen_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
dc.contributor.chairMeuillet, Emmanuelle J.en_US
dc.identifier.oclc659747368en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.levelmastersen_US
dc.contributor.committeememberHeimark, Ronald L.en_US
dc.contributor.committeememberGarver, William S.en_US
dc.identifier.proquest2192en_US
thesis.degree.disciplineNutritional Sciencesen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.nameMSen_US
refterms.dateFOA2018-08-24T17:02:59Z
html.description.abstractResearch has identified a linear relationship between saturated fat intake and colon cancer, and has demonstrated that high fat diets enhance tumorigenesis through elevation of secondary bile acids such as deoxycholic acid (DCA). We and others have shown that DCA can manipulate cell adhesion by decreasing expression of E-cadherin and increasing expression of beta-catenin. We have also shown that DCA significantly reduces EphB2 expression, which regulates cell positioning and segregation. Importantly, vitamin D can reinstate membranous E-cadherin/beta-catenin interactions and increase E-cadherin expression. In the present study, we sought to analyze the effects of DCA and vitamin D (cholecalciferol) treatment on EphB2 in colorectal cancer cells. Pre-treatment with cholecalciferol restored EphB2 expression in a dose-dependent manner, even with combined DCA treatment. This observation may be EGFR-dependent, suggesting that cholecalciferol may antagonize the effects of DCA. Taken together, these results suggest that cholecalciferol may represent an adjuvant therapy for colorectal cancer patients.


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