Focal adhesion kinase is required for KSHV vGPCR signaling.
Mol Carcinog
; 51(4): 339-51, 2012 Apr.
Article
em En
| MEDLINE
| ID: mdl-21538577
ABSTRACT
Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma, an angiogenic and inflammatory endothelial cell (EC) tumor that is common in areas of high KSHV prevalence. KSHV encodes a pro-angiogenic viral chemokine receptor (vGPCR) that promotes EC growth in vitro and KS-like tumors in mouse models. vGPCR is therefore considered a viral oncogene that plays a crucial role in the pathobiology of KS. In this study, we show that focal adhesion kinase (FAK) becomes activated upon vGPCR expression in primary ECs and that FAK is required for vGPCR-mediated activation of ERK1/2, NFκB, AP-1, and vGPCR-induced migration and inhibition of anoikis. FAK is crucial to cell motility and tumor invasiveness and is a potential therapeutic target in various malignancies. Our data show that via vGPCR, KSHV has evolved a way to constitutively activate FAK signaling.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Herpesvirus Humano 8
/
Receptores Acoplados a Proteínas G
/
Quinase 1 de Adesão Focal
Tipo de estudo:
Risk_factors_studies
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Mol Carcinog
Assunto da revista:
BIOLOGIA MOLECULAR
/
NEOPLASIAS
Ano de publicação:
2012
Tipo de documento:
Article