Differing Mechanisms of Death Induction by Fluorinated Taxane SB-T-12854 in Breast Cancer Cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F17%3A43913153" target="_blank" >RIV/00216208:11120/17:43913153 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.21873/anticanres.11488" target="_blank" >http://dx.doi.org/10.21873/anticanres.11488</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.21873/anticanres.11488" target="_blank" >10.21873/anticanres.11488</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Differing Mechanisms of Death Induction by Fluorinated Taxane SB-T-12854 in Breast Cancer Cells

Popis výsledku v původním jazyce

Background/Aim: Classical taxanes are routinely used in cancer therapy. In this study, mechanisms involved in death induction by novel fluorine-containing taxane SBT-12854 were investigated. Materials and Methods: We employed breast cancer SK-BR-3, MCF-7 and T47D cell lines to assess activation of individual caspases, changes in the expression of proteins of the Bcl-2 family, and the release of pro-apoptotic factors from mitochondria into the cytosol after SB-T-12854 treatment. Results: Caspase-2, -8, and -9 were activated in SK-BR-3 and MCF-7 cells. Only caspase8 was activated in T47D cells. Caspase-7 and -6 were activated in all tested cells while caspase-3 was activated only in SK-BR-3 cells. Pro-apoptotic Bad protein seems to be important for cell death induction in all tested cells. Antiapoptotic Bcl-2 and pro-apoptotic Bim, Bok, Bid and Bik seem to be also associated with cell death induction in some of the tested cells. The mitochondrial apoptotic pathway was significantly activated in association with the release of cytochrome c and Smac from mitochondria, but only in SKBR-3 cells, not in MCF-7 and T47D cells. Conclusion: Cell death induced by SB-T-12854, in the tested breast cancer cells, differs regarding activation of caspases, changes in levels of pro-apoptotic and anti-apoptotic proteins of the Bcl2 family and activation of the mitochondrial apoptotic pathway.

Název v anglickém jazyce

Differing Mechanisms of Death Induction by Fluorinated Taxane SB-T-12854 in Breast Cancer Cells

Popis výsledku anglicky

Background/Aim: Classical taxanes are routinely used in cancer therapy. In this study, mechanisms involved in death induction by novel fluorine-containing taxane SBT-12854 were investigated. Materials and Methods: We employed breast cancer SK-BR-3, MCF-7 and T47D cell lines to assess activation of individual caspases, changes in the expression of proteins of the Bcl-2 family, and the release of pro-apoptotic factors from mitochondria into the cytosol after SB-T-12854 treatment. Results: Caspase-2, -8, and -9 were activated in SK-BR-3 and MCF-7 cells. Only caspase8 was activated in T47D cells. Caspase-7 and -6 were activated in all tested cells while caspase-3 was activated only in SK-BR-3 cells. Pro-apoptotic Bad protein seems to be important for cell death induction in all tested cells. Antiapoptotic Bcl-2 and pro-apoptotic Bim, Bok, Bid and Bik seem to be also associated with cell death induction in some of the tested cells. The mitochondrial apoptotic pathway was significantly activated in association with the release of cytochrome c and Smac from mitochondria, but only in SKBR-3 cells, not in MCF-7 and T47D cells. Conclusion: Cell death induced by SB-T-12854, in the tested breast cancer cells, differs regarding activation of caspases, changes in levels of pro-apoptotic and anti-apoptotic proteins of the Bcl2 family and activation of the mitochondrial apoptotic pathway.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10608 - Biochemistry and molecular biology

Projekt

—

Návaznosti

S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Anticancer Research

ISSN

0250-7005

e-ISSN

—

Svazek periodika

37

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

GR - Řecká republika

Počet stran výsledku

10

Strana od-do

1581-1590

Kód UT WoS článku

000402167700006

EID výsledku v databázi Scopus

2-s2.0-85017478998