Cytotoxic drug induced JNK activation is DR5-dependent and vital for apoptosis and provides a new target for MSC-mediated delivery of DR5-specific sTRAIL variants
|dc.description.abstract||Over 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.subject||National Centre for Biomedical Engineering and Science (NCBES)||en_US|
|dc.title||Cytotoxic drug induced JNK activation is DR5-dependent and vital for apoptosis and provides a new target for MSC-mediated delivery of DR5-specific sTRAIL variants||en_US|
|dc.local.note||We 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 XIAP||en_US|
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