Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/13290
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dc.titleAnti-cancer mechanisms of indirubin-3'-monoxime
dc.contributor.authorSHI JIE
dc.date.accessioned2010-04-08T10:31:41Z
dc.date.available2010-04-08T10:31:41Z
dc.date.issued2008-04-28
dc.identifier.citationSHI JIE (2008-04-28). Anti-cancer mechanisms of indirubin-3'-monoxime. ScholarBank@NUS Repository.
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/13290
dc.description.abstractIndirubin-3b -monoxime (I3M) is a derivative of indirubin, an active component from a Chinese medicinal recipe with known anti-cancer function. In this study, we focused on the molecular mechanism underlying I3M-induced apoptosis, especially the critical role of the pro-apoptosis Bcl-2 family members. We first observed I3M-induced apoptosis in a time- and dose-dependent manner in three different types of human cancer cells. Induction of the caspase cascade for both the extrinsic and intrinsic pathways was demonstrated. Initiation of the death receptor pathway started with enhanced surface expression and protein level of DR4 and DR5, which correlated with the up-regulation of p53 and its transcriptional activity. Importantly, in HeLa cells caspase-8 activation resulted in Bid cleavage, followed by Bax conformational change. Consistently, stable knockdown of Bid abrogated I3M-induced Bax conformational change and cell death. Moreover, ectopic expression of a viral caspase inhibitor or Bcl-2 partially protected I3M-induced apoptosis.
dc.language.isoen
dc.subjectindirubin-3'-monoxime; death receptor; Bid; Bax; Apoptosis
dc.typeThesis
dc.contributor.departmentCOMMUNITY,OCCUPATIONAL & FAMILY MEDICINE
dc.contributor.supervisorSHEN HAN MING
dc.description.degreeMaster's
dc.description.degreeconferredMASTER OF SCIENCE
dc.identifier.isiutNOT_IN_WOS
Appears in Collections:Master's Theses (Open)

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