BRAF and RAS oncogenes regulate Rho GTPase pathways to mediate migration and invasion properties in human colon cancer cells: a comparative study
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F11%3A00371711" target="_blank" >RIV/68378050:_____/11:00371711 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1186/1476-4598-10-118" target="_blank" >http://dx.doi.org/10.1186/1476-4598-10-118</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1186/1476-4598-10-118" target="_blank" >10.1186/1476-4598-10-118</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
BRAF and RAS oncogenes regulate Rho GTPase pathways to mediate migration and invasion properties in human colon cancer cells: a comparative study
Popis výsledku v původním jazyce
Colorectal cancer is a common disease that involves genetic alterations, such as inactivation of tumour suppressor genes and activation of oncogenes such as or BRAF. The aim of this study is to dissect cell migration and invasion pathways that are utilised by BRAFV600E and mutated RAS oncoproteins. Colon adenocarcinoma cells with endogenous as well as ectopically expressed or silenced oncogenic mutations of BRAFV600E, KRASG12V and HRASG12V were employed. BRAFV600E significantly induces cell migration and invasion of colon cancer cells partly via activation of RhoA GTPase. KRASG12V enhances the ability of colon adenocarcinoma cells Caco-2 to migrate and invade through filopodia formation. Increased cell migration and invasion, mediated by Rac1 and mesenchymal morphology were the main characteristics rendered by HRASG12V in Caco-2 cells. RAS oncogenes can also cooperate with the TGFbeta-1 pathway in cellular transformation.
Název v anglickém jazyce
BRAF and RAS oncogenes regulate Rho GTPase pathways to mediate migration and invasion properties in human colon cancer cells: a comparative study
Popis výsledku anglicky
Colorectal cancer is a common disease that involves genetic alterations, such as inactivation of tumour suppressor genes and activation of oncogenes such as or BRAF. The aim of this study is to dissect cell migration and invasion pathways that are utilised by BRAFV600E and mutated RAS oncoproteins. Colon adenocarcinoma cells with endogenous as well as ectopically expressed or silenced oncogenic mutations of BRAFV600E, KRASG12V and HRASG12V were employed. BRAFV600E significantly induces cell migration and invasion of colon cancer cells partly via activation of RhoA GTPase. KRASG12V enhances the ability of colon adenocarcinoma cells Caco-2 to migrate and invade through filopodia formation. Increased cell migration and invasion, mediated by Rac1 and mesenchymal morphology were the main characteristics rendered by HRASG12V in Caco-2 cells. RAS oncogenes can also cooperate with the TGFbeta-1 pathway in cellular transformation.
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
EB - Genetika a molekulární biologie
OECD FORD obor
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Návaznosti výsledku
Projekt
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Návaznosti
Z - Vyzkumny zamer (s odkazem do CEZ)
Ostatní
Rok uplatnění
2011
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Molecular Cancer
ISSN
1476-4598
e-ISSN
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Svazek periodika
10
Číslo periodika v rámci svazku
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Stát vydavatele periodika
GB - Spojené království Velké Británie a Severního Irska
Počet stran výsledku
21
Strana od-do
"e118"
Kód UT WoS článku
000295831300001
EID výsledku v databázi Scopus
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