Focal Adhesion Kinase functions as an Akt downstream target in migration of colorectal cancer cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F09%3A00335669" target="_blank" >RIV/68378050:_____/09:00335669 - isvavai.cz</a>

Výsledek na webu

—

DOI - Digital Object Identifier

—

Jazyk výsledku

angličtina

Název v původním jazyce

Focal Adhesion Kinase functions as an Akt downstream target in migration of colorectal cancer cells

Popis výsledku v původním jazyce

Migration plays a crucial role in cancer cell invasion and metastasis. The focus of this study is the collaboration of Akt, FAK and Src kinases in migration and invasion of colorectal cancer cells. We show that all three kinases can be found in one protein complex but the interaction between Akt and Src is indirect and mediated by FAK. Interestingly, induced Akt signaling causes an increased tyrosine phosphorylation of FAK but this increase is attenuated by Src inhibitor SU6656. We also show that activeAkt stimulates cell migration, but this phenomenon is blocked by FAK knockdown or by inhibition of Src kinase. In addition, all three kinases appeared crucial for successful invasion of colorectal cancer cells. Alltogether, our data suggest the mechanism how the pathway can affect migration of colorectal adenocarcinoma cells. Since FAK acts downstream of Akt, our results imply FAK kinase as a potential key molecule during progression of tumors with active PI3-K/Akt signaling.

Název v anglickém jazyce

Focal Adhesion Kinase functions as an Akt downstream target in migration of colorectal cancer cells

Popis výsledku anglicky

Migration plays a crucial role in cancer cell invasion and metastasis. The focus of this study is the collaboration of Akt, FAK and Src kinases in migration and invasion of colorectal cancer cells. We show that all three kinases can be found in one protein complex but the interaction between Akt and Src is indirect and mediated by FAK. Interestingly, induced Akt signaling causes an increased tyrosine phosphorylation of FAK but this increase is attenuated by Src inhibitor SU6656. We also show that activeAkt stimulates cell migration, but this phenomenon is blocked by FAK knockdown or by inhibition of Src kinase. In addition, all three kinases appeared crucial for successful invasion of colorectal cancer cells. Alltogether, our data suggest the mechanism how the pathway can affect migration of colorectal adenocarcinoma cells. Since FAK acts downstream of Akt, our results imply FAK kinase as a potential key molecule during progression of tumors with active PI3-K/Akt signaling.

Druh

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

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

—

Projekt

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

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2009

Kód důvěrnosti údajů

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

Název periodika

Translational Oncology

ISSN

1936-5233

e-ISSN

—

Svazek periodika

2

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

—

Kód UT WoS článku

—

EID výsledku v databázi Scopus

—