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Statements

Subject Item
n2:RIV%2F00216208%3A11120%2F15%3A43909312%21RIV15-MSM-11120___
rdf:type
n9:Vysledek skos:Concept
dcterms:description
Background: In previous study we showed that caspase-2 plays the role of an apical caspase in cell death induction by taxanes in breast cancer cells. This study deals with the role of other caspases. We tested breast cancer cell lines SK-BR-3 (functional caspase-3) and MCF-7 (nonfunctional caspase-3). Methods and Results: Using western blot analysis we demonstrated the activation of initiator caspase-8 and -9 as well as executioner caspase-6 and -7 in both tested cell lines after application of taxanes (paclitaxel, SB-T-1216) at death-inducing concentrations. Caspase-3 activation was also found in SK-BR-3 cells. Employing specific siRNAs after taxane application, suppression of caspase-3 expression significantly increased the number of surviving SK-BR-3 cells. Inhibition of caspase-7 expression also increased the number of surviving SK-BR-3 and MCF-7 cells. On the other hand, suppression of caspase-8 and caspase-9 expression had no significant effect on cell survival. However, caspase-9 seemed to be involved in the activation of caspase-3 and caspase-7. Caspase-3 and caspase-7 appeared to activate mutually. Furthermore, we observed a significant decrease in mitochondrial membrane potential (flow cytometric analysis) and cytochrome c release (confocal microscopy, western blot after cell fractionation) from mitochondria in SK-BR-3 cells. No such changes were observed in MCF-7 cells after taxane treatment. Conclusion: We conclude that the activation of apical caspase-2 results in the activation of caspase-3 and -7 without the involvement of mitochondria. Caspase-9 can be activated directly via caspase-2 or alternatively after cytochrome c release from mitochondria. Subsequently, caspase-9 activation can also lead to caspase-3 and -7 activation. Caspase-3 and caspase-7 activate mutually. It seems that there is also a parallel pathway involving mitochondria that can cooperate in taxane-induced cell death in breast cancer cells. Background: In previous study we showed that caspase-2 plays the role of an apical caspase in cell death induction by taxanes in breast cancer cells. This study deals with the role of other caspases. We tested breast cancer cell lines SK-BR-3 (functional caspase-3) and MCF-7 (nonfunctional caspase-3). Methods and Results: Using western blot analysis we demonstrated the activation of initiator caspase-8 and -9 as well as executioner caspase-6 and -7 in both tested cell lines after application of taxanes (paclitaxel, SB-T-1216) at death-inducing concentrations. Caspase-3 activation was also found in SK-BR-3 cells. Employing specific siRNAs after taxane application, suppression of caspase-3 expression significantly increased the number of surviving SK-BR-3 cells. Inhibition of caspase-7 expression also increased the number of surviving SK-BR-3 and MCF-7 cells. On the other hand, suppression of caspase-8 and caspase-9 expression had no significant effect on cell survival. However, caspase-9 seemed to be involved in the activation of caspase-3 and caspase-7. Caspase-3 and caspase-7 appeared to activate mutually. Furthermore, we observed a significant decrease in mitochondrial membrane potential (flow cytometric analysis) and cytochrome c release (confocal microscopy, western blot after cell fractionation) from mitochondria in SK-BR-3 cells. No such changes were observed in MCF-7 cells after taxane treatment. Conclusion: We conclude that the activation of apical caspase-2 results in the activation of caspase-3 and -7 without the involvement of mitochondria. Caspase-9 can be activated directly via caspase-2 or alternatively after cytochrome c release from mitochondria. Subsequently, caspase-9 activation can also lead to caspase-3 and -7 activation. Caspase-3 and caspase-7 activate mutually. It seems that there is also a parallel pathway involving mitochondria that can cooperate in taxane-induced cell death in breast cancer cells.
dcterms:title
The role of individual caspases in cell death induction by taxanes in breast cancer cells The role of individual caspases in cell death induction by taxanes in breast cancer cells
skos:prefLabel
The role of individual caspases in cell death induction by taxanes in breast cancer cells The role of individual caspases in cell death induction by taxanes in breast cancer cells
skos:notation
RIV/00216208:11120/15:43909312!RIV15-MSM-11120___
n3:aktivita
n16:P n16:I
n3:aktivity
I, P(GA301/09/0362)
n3:cisloPeriodika
1
n3:dodaniDat
n8:2015
n3:domaciTvurceVysledku
n6:7090277 n6:5621879 n6:8055149 n6:4215036 n6:4220803 n6:8486824 n6:1758330
n3:druhVysledku
n12:J
n3:duvernostUdaju
n10:S
n3:entitaPredkladatele
n13:predkladatel
n3:idSjednocenehoVysledku
406
n3:idVysledku
RIV/00216208:11120/15:43909312
n3:jazykVysledku
n17:eng
n3:klicovaSlova
cell death; caspases; breast cancer; taxanes
n3:klicoveSlovo
n7:taxanes n7:breast%20cancer n7:caspases n7:cell%20death
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[4E06DE101F19]
n3:nazevZdroje
Cancer Cell International
n3:obor
n14:EB
n3:pocetDomacichTvurcuVysledku
7
n3:pocetTvurcuVysledku
9
n3:projekt
n19:GA301%2F09%2F0362
n3:rokUplatneniVysledku
n8:2015
n3:svazekPeriodika
15
n3:tvurceVysledku
Zanardi, Ilaria Balušíková, Kamila Ojima, Iwao Šrámek, Jan Schmiedlová, Martina Stančíková, Jitka Jelínek, Michael Kovář, Jan Němcová-Fürstová, Vlasta
n3:wos
000350172000001
s:issn
1475-2867
s:numberOfPages
16
n15:doi
10.1186/s12935-015-0155-7
n18:organizacniJednotka
11120