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• W2061035214 abstract "Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anticancer agent as it selectively kills tumor cells but spares normal cells. Resistance to TRAIL by tumor cells limits its therapeutic use. We have previously shown that protein kinase C-ɛ (PKCɛ) acts as an antiapoptotic protein in MCF-7 breast cancer cells. In the present study, we have investigated the mechanism(s) by which PKCɛ contributes to TRAIL resistance. Overexpression of PKCɛ inhibited caspase-8 and -9 activation, release of mitochondrial cytochrome c and cell death induced by TRAIL, but did not interfere with the recruitment of caspase-8 to the death-inducing signaling complex. Knockdown/inhibition of PKCɛ resulted in enhanced sensitivity to TRAIL. The level of Bcl-2 was increased and Bid was decreased by PKCɛ at both the protein and mRNA level but PKCɛ had no effect on Bax. Knockdown of Bcl-2 by siRNA reversed TRAIL resistance in PKCɛ-overexpressing cells, whereas depletion of Bid contributed to TRAIL resistance in MCF-7 cells. A decrease in Bid content was also associated with inhibition of TRAIL-induced caspase-8 activation. Furthermore, PKCɛ depletion or overexpression of DN-PKCɛ was associated with a decrease in Bcl-2 protein level. Thus, our results suggest that PKCɛ acts upstream of mitochondria and mediates TRAIL resistance via both Bcl-2 and Bid in MCF-7 cells." @default.
• W2061035214 created "2016-06-24" @default.
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• W2061035214 date "2006-12-22" @default.
• W2061035214 modified "2023-10-16" @default.
• W2061035214 title "Downregulation of Bid is associated with PKCɛ-mediated TRAIL resistance" @default.
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• W2061035214 doi "https://doi.org/10.1038/sj.cdd.4402077" @default.
• W2061035214 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17186022" @default.
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