Diferenciace buněk kolorektálního karcinomu vyvolaná butyrátem sodným: regulace PKC-betaII PI3-kinázou

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F05%3A00000231" target="_blank" >RIV/68378050:_____/05:00000231 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Sodium butyrate-mediated differentiation of colorectal cancer cells: regulation of PKC-betaII by PI3-kinase

Popis výsledku v původním jazyce

The study focuses on a putative regulation of PKCbII by PI 3-kinase in colorectal adenocarcinoma cells. We examined the activity of PI 3-kinase in HT29 cells that differentiate after stimulation with appropriate agents, and in Caco-2 cells differentiating spontaneously. The activity of PI3-kinase and PKCbII decreased in sodium butyrate-stimulated HT29 cells. In HT29 cells infected with adenovirus encoding constitutively active PI 3-kinase, the activity of alkaline phosphatase was blocked, and this PI 3-kinase potentiated the activity of PKCbII in HT29 cells despite the presence of NaBT in the culture medium. On the contrary, in Caco-2 cells, the activity of PI3-kinase was not butyrate-sensitive. Also, the alkaline phosphatase activity was not affectedby the ectopic PI 3-kinase in Caco-2 cells. Our findings suggest that PKCbII is regulated by PI 3-kinase in HT29 cells and that the mechanisms of spontaneous versus butyrate-induced differentiation of colorectal carcinoma cells may dif...

Název v anglickém jazyce

Sodium butyrate-mediated differentiation of colorectal cancer cells: regulation of PKC-betaII by PI3-kinase

Popis výsledku anglicky

The study focuses on a putative regulation of PKCbII by PI 3-kinase in colorectal adenocarcinoma cells. We examined the activity of PI 3-kinase in HT29 cells that differentiate after stimulation with appropriate agents, and in Caco-2 cells differentiating spontaneously. The activity of PI3-kinase and PKCbII decreased in sodium butyrate-stimulated HT29 cells. In HT29 cells infected with adenovirus encoding constitutively active PI 3-kinase, the activity of alkaline phosphatase was blocked, and this PI 3-kinase potentiated the activity of PKCbII in HT29 cells despite the presence of NaBT in the culture medium. On the contrary, in Caco-2 cells, the activity of PI3-kinase was not butyrate-sensitive. Also, the alkaline phosphatase activity was not affectedby the ectopic PI 3-kinase in Caco-2 cells. Our findings suggest that PKCbII is regulated by PI 3-kinase in HT29 cells and that the mechanisms of spontaneous versus butyrate-induced differentiation of colorectal carcinoma cells may dif...

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

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2005

Kód důvěrnosti údajů

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

Název periodika

International Journal of Molecular Medicine

ISSN

1107-3756

e-ISSN

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Svazek periodika

15

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

GR - Řecká republika

Počet stran výsledku

7

Strana od-do

329-335

Kód UT WoS článku

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EID výsledku v databázi Scopus

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