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  • Title: Caspase-8 activation independent of CD95/CD95-L interaction during paclitaxel-induced apoptosis in human colon cancer cells (HT29-D4).
    Author: Gonçalves A, Braguer D, Carles G, André N, Prevôt C, Briand C.
    Journal: Biochem Pharmacol; 2000 Dec 01; 60(11):1579-84. PubMed ID: 11077039.
    Abstract:
    Antimicrotubule agent-induced apoptosis was examined in the proliferating human colon cancer cell line HT29-D4. G2/M arrest and subsequent apoptosis were dose-dependent, both observed with 100 nM paclitaxel or docetaxel and 10 nM vinorelbine. Bcl-x(L) phosphorylation was observed simultaneously with mitotic block, then caspase-3 cleavage and poly(ADP-ribose) polymerase degradation were detected 48 hr later. By using both enzymatic assay and immunoblot detection of cleaved fragments, we showed that caspase-8, a central component of the CD95-induced apoptotic pathway, was significantly activated during paclitaxel exposure, contemporary to apoptosis occurrence. Caspase-8 activation and apoptosis were independent of CD95 ligation and evidenced only for concentrations inducing Bcl-x(L) phosphorylation and a decrease in mitochondria permeability. Similar results were obtained with docetaxel and vinca alkaloids. Thus, antimitotic drugs may induce apoptosis via caspase-8 activation independently of CD95/CD95-L. Caspase-8 may be a common mediator of anticancer drug-induced apoptosis that could represent a promising target for future therapies.
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