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Statements

Subject Item
n2:RIV%2F00216208%3A11120%2F13%3A43907485%21RIV14-GA0-11120___
rdf:type
n11:Vysledek skos:Concept
dcterms:description
We studied the role of caspase-2 in apoptosis induction by taxanes (paclitaxel, novel taxane SB-T-1216) in breast cancer cells using SK-BR-3 and MCF-7 cell lines. Both taxanes induced apoptosis in SK-BR-3 as well as MCF-7 cells. Caspase-2 activity in SK-BR-3 cells increased approximately 15-fold within 48 h after the application of both taxanes at the death-inducing concentration (100 nM). In MCF-7 cells, caspase-2 activity increased approximately 11-fold within 60 h after the application of taxanes (300 nM). Caspase-2 activation was confirmed by decreasing levels of procaspase-2, increasing levels of cleaved caspase-2 and the cleavage of caspase-2 substrate golgin-160. The inhibition of caspase-2 expression using siRNA increased the number of surviving cells more than 2-fold in MCF-7 cells, and at least 4-fold in SK-BR-3 cells, 96 h after the application of death-inducing concentration of taxanes. The inhibition of caspase-2 expression also resulted in decreased cleavage of initiator caspases as well as executioner caspases in both cell lines after the application of taxanes. In control cells, caspase-2 seemed to be mainly localized in the nucleus. After the application of taxanes, it was released from the nucleus to the cytosol, due to the long-term disintegration of the nuclear envelope, in both cell lines. After taxane application, p21(WAF1/CIP1) expression was only induced in MCF-7 cells with functional p53. However, taxane application did not result in a significant increase of PIDD expression in either SK-BR-3 or MCF-7 cells. The inhibition of RAIDD expression using siRNA did not affect the number of surviving SK-BR-3 and MCF-7 cells after taxane application at all. Caspase-2 is required, at least partially, for apoptosis induction by taxanes in tested breast cancer cells. We suggest that caspase-2 plays the role of an apical caspase in these cells. We studied the role of caspase-2 in apoptosis induction by taxanes (paclitaxel, novel taxane SB-T-1216) in breast cancer cells using SK-BR-3 and MCF-7 cell lines. Both taxanes induced apoptosis in SK-BR-3 as well as MCF-7 cells. Caspase-2 activity in SK-BR-3 cells increased approximately 15-fold within 48 h after the application of both taxanes at the death-inducing concentration (100 nM). In MCF-7 cells, caspase-2 activity increased approximately 11-fold within 60 h after the application of taxanes (300 nM). Caspase-2 activation was confirmed by decreasing levels of procaspase-2, increasing levels of cleaved caspase-2 and the cleavage of caspase-2 substrate golgin-160. The inhibition of caspase-2 expression using siRNA increased the number of surviving cells more than 2-fold in MCF-7 cells, and at least 4-fold in SK-BR-3 cells, 96 h after the application of death-inducing concentration of taxanes. The inhibition of caspase-2 expression also resulted in decreased cleavage of initiator caspases as well as executioner caspases in both cell lines after the application of taxanes. In control cells, caspase-2 seemed to be mainly localized in the nucleus. After the application of taxanes, it was released from the nucleus to the cytosol, due to the long-term disintegration of the nuclear envelope, in both cell lines. After taxane application, p21(WAF1/CIP1) expression was only induced in MCF-7 cells with functional p53. However, taxane application did not result in a significant increase of PIDD expression in either SK-BR-3 or MCF-7 cells. The inhibition of RAIDD expression using siRNA did not affect the number of surviving SK-BR-3 and MCF-7 cells after taxane application at all. Caspase-2 is required, at least partially, for apoptosis induction by taxanes in tested breast cancer cells. We suggest that caspase-2 plays the role of an apical caspase in these cells.
dcterms:title
Caspase-2 is involved in cell death induction by taxanes in breast cancer cells Caspase-2 is involved in cell death induction by taxanes in breast cancer cells
skos:prefLabel
Caspase-2 is involved in cell death induction by taxanes in breast cancer cells Caspase-2 is involved in cell death induction by taxanes in breast cancer cells
skos:notation
RIV/00216208:11120/13:43907485!RIV14-GA0-11120___
n11:predkladatel
n12:orjk%3A11120
n3:aktivita
n16:P n16:I
n3:aktivity
I, P(GA301/09/0362)
n3:cisloPeriodika
42
n3:dodaniDat
n14:2014
n3:domaciTvurceVysledku
n15:4220803 n15:8055149 n15:1456695 n15:4215036 n15:1758330 n15:3568946 n15:7090277
n3:druhVysledku
n8:J
n3:duvernostUdaju
n17:S
n3:entitaPredkladatele
n10:predkladatel
n3:idSjednocenehoVysledku
64383
n3:idVysledku
RIV/00216208:11120/13:43907485
n3:jazykVysledku
n20:eng
n3:klicovaSlova
Breast cancer cells; Taxanes; Cell death; Caspase-2
n3:klicoveSlovo
n4:Breast%20cancer%20cells n4:Caspase-2 n4:Taxanes n4:Cell%20death
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[CCE3C963047F]
n3:nazevZdroje
Cancer Cell International
n3:obor
n19:FD
n3:pocetDomacichTvurcuVysledku
7
n3:pocetTvurcuVysledku
9
n3:projekt
n18:GA301%2F09%2F0362
n3:rokUplatneniVysledku
n14:2013
n3:svazekPeriodika
13
n3:tvurceVysledku
Šrámek, Jan Kopperová, Dana Fidlerová, Julie Němcová-Fürstová, Vlasta Jelínek, Michael Balušíková, Kamila Ojima, Iwao Zanardi, Ilaria Kovář, Jan
n3:wos
000320553000001
s:issn
1475-2867
s:numberOfPages
15
n13:doi
10.1186/1475-2867-13-42
n9:organizacniJednotka
11120