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dc.contributor.authorZhang, Xuan
dc.contributor.authorTimmermann, Barbara N.
dc.contributor.authorSamadi, Abbas K.
dc.contributor.authorCohen, Mark S.
dc.date.accessioned2015-05-11T19:59:47Z
dc.date.available2015-05-11T19:59:47Z
dc.date.issued2012-06-01
dc.identifier.citationZhang, X., Timmmerman, B. N., Samadi, A. & Cohen, M. (2012) Withaferin A Induces Proteasome-Dependent Degradation of Breast Cancer Susceptibility Gene 1 and Heat Shock Factor 1 Proteins in Breast Cancer Cells. ISRN Biochemistry, 2012, 6pg. http://www.dx.doi.org/10.5402/2012/707586en_US
dc.identifier.urihttp://hdl.handle.net/1808/17711
dc.descriptionThis is the publisher's version, also available electronically from "http://www.hindawi.com".en_US
dc.description.abstractThe purpose of this study was to examine the regulation of prosurvival factors heat shock factor 1 (HSF1) and breast cancer susceptibility gene 1 (BRCA1) by a natural withanolide withaferin A (WA) in triple negative breast cancer cell lines MDA-MB-231 and BT20. Western analysis was used to examine alternations in HSF1 and BRCA1 protein levels following WA treatment. A protein synthesis inhibitor cycloheximide and a proteasome inhibitor MG132 were used to investigate the mechanisms of HSF1 and BRCA1 regulation by WA. It was found that WA induced a dose-dependent decrease in HSF1 and BRCA1 protein levels. Further analysis showed that levels of HSF1 and BRCA1 proteins decreased rapidly after WA treatment, and this was attributed to WA-induced denaturation of HSF1 and BRCA1 proteins and subsequent degradation via proteasome-dependent, and protein-synthesis dependent mechanism. In summary, WA induces denaturation and proteasomal degradation of HSF1 and BRCA1 proteins. Further studies are warranted to examine the contribution of HSF1 and BRCA1 depletion to the anticancer effects of WA in breast cancer.en_US
dc.publisherHindawi Publishing Corporationen_US
dc.titleWithaferin A Induces Proteasome-Dependent Degradation of Breast Cancer Susceptibility Gene 1 and Heat Shock Factor 1 Proteins in Breast Cancer Cellsen_US
dc.typeArticle
kusw.kuauthorTimmermann, Barbara N.
kusw.kudepartmentMedicinal Chemistryen_US
dc.identifier.doi10.5402/2012/707586
kusw.oaversionScholarly/refereed, publisher version
kusw.oapolicyThis item meets KU Open Access policy criteria.
dc.rights.accessrightsopenAccess


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