Changes in the response of MCF-7 cells to ionizing radiation after the combination of ATM and DNA-PK inhibition

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F15%3A10293814" target="_blank" >RIV/00216208:11150/15:10293814 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/60162694:G44__/15:43875359 RIV/00216275:25310/15:39900079

Výsledek na webu

<a href="http://link.springer.com/article/10.1007%2Fs12032-015-0591-1" target="_blank" >http://link.springer.com/article/10.1007%2Fs12032-015-0591-1</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s12032-015-0591-1" target="_blank" >10.1007/s12032-015-0591-1</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Changes in the response of MCF-7 cells to ionizing radiation after the combination of ATM and DNA-PK inhibition

Popis výsledku v původním jazyce

The aim of the present study is to evaluate the role of ATM (KU55933) and DNA-PK (NU7441) inhibitors in the repair of double-strand breaks and downstream signaling of DNA damage introduced by ionizing radiation. The irradiation of MCF-7 cells alone increased the proportion of cells in the G1 phase in comparison with mock-treated cells. After ATM inhibitor pretreatment, the cells were more accumulated in the G2 phase, whereas DNA-PK inhibitor application increased the percentage of cells in the G1 phase.ATM and DNA-PK inhibitor application alone increased the sensitivity of MCF-7 cells to ionizing radiation; however, combining both inhibitors together resulted in a further enhancement of cell death. Unexpectedly, combining both inhibitors decreased thepercentage of senescent cells and increased G2 cell cycle arrest 3 days after treatment. After irradiation, the p21 protein was increased and Chk1 and Chk2 were activated. These proteins were not increased in cells pretreated with the AT

Název v anglickém jazyce

Changes in the response of MCF-7 cells to ionizing radiation after the combination of ATM and DNA-PK inhibition

Popis výsledku anglicky

The aim of the present study is to evaluate the role of ATM (KU55933) and DNA-PK (NU7441) inhibitors in the repair of double-strand breaks and downstream signaling of DNA damage introduced by ionizing radiation. The irradiation of MCF-7 cells alone increased the proportion of cells in the G1 phase in comparison with mock-treated cells. After ATM inhibitor pretreatment, the cells were more accumulated in the G2 phase, whereas DNA-PK inhibitor application increased the percentage of cells in the G1 phase.ATM and DNA-PK inhibitor application alone increased the sensitivity of MCF-7 cells to ionizing radiation; however, combining both inhibitors together resulted in a further enhancement of cell death. Unexpectedly, combining both inhibitors decreased thepercentage of senescent cells and increased G2 cell cycle arrest 3 days after treatment. After irradiation, the p21 protein was increased and Chk1 and Chk2 were activated. These proteins were not increased in cells pretreated with the AT

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

CE - Biochemie

OECD FORD obor

—

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2015

Kód důvěrnosti údajů

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

Název periodika

Medical Oncology

ISSN

1357-0560

e-ISSN

—

Svazek periodika

32

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

8

Strana od-do

—

Kód UT WoS článku

000352152000002

EID výsledku v databázi Scopus

2-s2.0-84925590335