Loss of PTEN Facilitates Rosiglitazone-Mediated Enhancement of Platinum(IV) Complex LA-12-Induced Apoptosis in Colon Cancer Cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F15%3A00452062" target="_blank" >RIV/68081707:_____/15:00452062 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00179906:_____/15:10314407 RIV/00216224:14310/15:00095868

Výsledek na webu

<a href="http://dx.doi.org/10.1371/journal.pone.0141020" target="_blank" >http://dx.doi.org/10.1371/journal.pone.0141020</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1371/journal.pone.0141020" target="_blank" >10.1371/journal.pone.0141020</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Loss of PTEN Facilitates Rosiglitazone-Mediated Enhancement of Platinum(IV) Complex LA-12-Induced Apoptosis in Colon Cancer Cells

Popis výsledku v původním jazyce

We demonstrated for the first time an outstanding ability of rosiglitazone to mediate a profound enhancement of LA-12-induced apoptosis associated with activation of mitochondrial pathway in human colon cancer cells. This effect was preferentially observed in the G1 cell cycle phase, independent on p53 and PPAR. proteins, and accompanied with significant changes of selected Bcl-2 family protein levels. Further stimulation of cooperative synergic cytotoxic action of rosiglitazone and LA-12 was demonstrated in the cells deficient for PTEN, where mitochondrial apoptotic pathway was more stimulated and G1-phase-associated dying was reinforced. Our results suggest that combined treatment with rosiglitazone and LA-12 might be promising anticancer strategy incolon-derived tumours regardless of their p53 status, and also favourable in those defective in PTEN function.

Název v anglickém jazyce

Loss of PTEN Facilitates Rosiglitazone-Mediated Enhancement of Platinum(IV) Complex LA-12-Induced Apoptosis in Colon Cancer Cells

Popis výsledku anglicky

We demonstrated for the first time an outstanding ability of rosiglitazone to mediate a profound enhancement of LA-12-induced apoptosis associated with activation of mitochondrial pathway in human colon cancer cells. This effect was preferentially observed in the G1 cell cycle phase, independent on p53 and PPAR. proteins, and accompanied with significant changes of selected Bcl-2 family protein levels. Further stimulation of cooperative synergic cytotoxic action of rosiglitazone and LA-12 was demonstrated in the cells deficient for PTEN, where mitochondrial apoptotic pathway was more stimulated and G1-phase-associated dying was reinforced. Our results suggest that combined treatment with rosiglitazone and LA-12 might be promising anticancer strategy incolon-derived tumours regardless of their p53 status, and also favourable in those defective in PTEN function.

Druh

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

CEP obor

BO - Biofyzika

OECD FORD obor

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Projekt

<a href="/cs/project/GA15-06650S" target="_blank" >GA15-06650S: Nové molekulární mechanismy smrti nádorových buněk indukované chemoterapeutickými látkami a cytokiny</a><br>

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

PLoS ONE

ISSN

1932-6203

e-ISSN

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Svazek periodika

10

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

20

Strana od-do

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Kód UT WoS článku

000363249300023

EID výsledku v databázi Scopus

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