The role of p38 in irinotecan-induced DNA damage and apoptosis of colon cancer cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F13%3A10133987" target="_blank" >RIV/00216208:11150/13:10133987 - isvavai.cz</a>

Výsledek na webu

<a href="http://www.sciencedirect.com/science/article/pii/S0027510713000158" target="_blank" >http://www.sciencedirect.com/science/article/pii/S0027510713000158</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.mrfmmm.2013.02.002" target="_blank" >10.1016/j.mrfmmm.2013.02.002</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The role of p38 in irinotecan-induced DNA damage and apoptosis of colon cancer cells

Popis výsledku v původním jazyce

The role of p38 in irinotecan (CPT-11)-induced damage and cell death in colon cancer cell line SW620 was investigated. We demonstrate that CPT-11 treatment activates p38 in exposed cells, however with concentration dependent dynamics and differing consequences. Higher CPT-11 concentrations induce a massive early but relatively short-lasting p38 activity leading to apoptosis mediated by mitochondria and caspases. Pharmacological or siRNA inhibition of p38 then significantly prevents CPT-11-dependent celldeath. Conversely, lower CPT-11 concentrations activate p38 in a delayed, however sustained manner, with apoptosis occurring only in a fraction of cells and in the absence of significant autophagy. Blocking p38 in thus treated cells increases their sensitivity toward CPT-11 and increases cell death. In summary, our results confirm the involvement of p38 in colon cancer cells response to CPT-11 while indicating a varying role of p38 in the final biological response.

Název v anglickém jazyce

The role of p38 in irinotecan-induced DNA damage and apoptosis of colon cancer cells

Popis výsledku anglicky

The role of p38 in irinotecan (CPT-11)-induced damage and cell death in colon cancer cell line SW620 was investigated. We demonstrate that CPT-11 treatment activates p38 in exposed cells, however with concentration dependent dynamics and differing consequences. Higher CPT-11 concentrations induce a massive early but relatively short-lasting p38 activity leading to apoptosis mediated by mitochondria and caspases. Pharmacological or siRNA inhibition of p38 then significantly prevents CPT-11-dependent celldeath. Conversely, lower CPT-11 concentrations activate p38 in a delayed, however sustained manner, with apoptosis occurring only in a fraction of cells and in the absence of significant autophagy. Blocking p38 in thus treated cells increases their sensitivity toward CPT-11 and increases cell death. In summary, our results confirm the involvement of p38 in colon cancer cells response to CPT-11 while indicating a varying role of p38 in the final biological response.

Druh

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

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2013

Kód důvěrnosti údajů

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

Název periodika

Mutation Research

ISSN

0027-5107

e-ISSN

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Svazek periodika

741-742

Číslo periodika v rámci svazku

January - February

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

8

Strana od-do

27-34

Kód UT WoS článku

000318456400004

EID výsledku v databázi Scopus

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