作者: Michael Jelínek , Kamila Balušíková , Martina Schmiedlová , Vlasta Němcová-Fürstová , Jan Šrámek
DOI: 10.1186/S12935-015-0155-7
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摘要: In previous study we showed that caspase-2 plays the role of an apical caspase in cell death induction by taxanes breast cancer cells. This deals with other caspases. We tested lines SK-BR-3 (functional caspase-3) and MCF-7 (nonfunctional caspase-3). Using western blot analysis demonstrated activation initiator caspase-8 -9 as well executioner caspase-6 -7 both after application (paclitaxel, SB-T-1216) at death-inducing concentrations. Caspase-3 was also found Employing specific siRNAs taxane application, suppression caspase-3 expression significantly increased number surviving Inhibition caspase-7 On hand, caspase-9 had no significant effect on survival. However, seemed to be involved caspase-7. appeared activate mutually. Furthermore, observed a decrease mitochondrial membrane potential (flow cytometric analysis) cytochrome c release (confocal microscopy, fractionation) from mitochondria No such changes were cells treatment. conclude results without involvement mitochondria. Caspase-9 can activated directly via or alternatively Subsequently, lead activations. It seems there is parallel pathway involving cooperate taxane-induced