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dc.contributor.advisorZwacka, Ralf
dc.contributor.authorRui, Yu
dc.date.accessioned2013-07-16T12:13:51Z
dc.date.available2013-10-08T17:22:44Z
dc.date.issued2013-03-20
dc.identifier.urihttp://hdl.handle.net/10379/3519
dc.description.abstractOver the past two decades, cancer research has produced tremendous advances in our understanding of the pathogenesis of cancer. Among the most important of these advances is the realization that apoptosis and the proteins involved in this process of it have a profound effect on the development of malignancies. This study is composed of two parts, in part I we found JNK activation is DR5-dependent and it can regulate apoptosis via Bid phosphorylation in HCT116 colorectal cancer cells after treatment with the chemotherapeutic agent 5-FU (5-fluorouracil). In part II we designed a form of soluble TRAIL (TNF-related apoptosis-inducing ligand), which can be delivered by MSCs (mesenchymal stem cells) and showed enhanced apoptosis-inducing activity in combination with 5-FU or silencing of XIAP (X-linked inhibitor of apoptosis protein). All these findings provide more insights into the mechanism of apoptosis and may be helpful to design better therapeutic approaches.en_US
dc.subjectApoptosisen_US
dc.subjectDR5en_US
dc.subject5-FUen_US
dc.subjectTRAILen_US
dc.subjectMSCen_US
dc.subjectNational Centre for Biomedical Engineering and Science (NCBES)en_US
dc.titleCytotoxic drug induced JNK activation is DR5-dependent and vital for apoptosis and provides a new target for MSC-mediated delivery of DR5-specific sTRAIL variantsen_US
dc.typeThesisen_US
dc.local.noteWe found JNK activation is DR5-dependent and it can regulate apoptosis via Bid phosphorylation in HCT116 cells after treatment with the 5-FU. In addition we designed a form of soluble TRAIL, which can be delivered by MSCs and showed enhanced apoptosis-inducing activity in combination with 5-FU or silencing of XIAPen_US
dc.local.finalYesen_US
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