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Construction of stable focal adhesion kinase knockdown cell line and preliminary study of its properties / 药学学报
Acta Pharmaceutica Sinica ; (12): 1128-1133, 2012.
Artigo em Chinês | WPRIM | ID: wpr-274688
ABSTRACT
Malignant melanoma still remains to be a serious health threat. Overexpression of focal adhesion kinase (FAK) in melanoma has suggested that FAK could be a promising target for therapeutic intervention. To further investigate the function of FAK in melanoma, FAK expression was down-regulated by stable transfection of plasmid harboring FAK small interfering RNA (siRNA) into melanoma cell line. Two stable cell lines, F10-siFAK and F10-control, have been constructed and screened. Compared with the F10-control, both the mRNA and protein levels of FAK decreased significantly, and the cell cycle of F10-siFAK was arrested at G1 phase. Furthermore, the tumor growth rate of F10-siFAK cells was notably slower than that of F10-control in in vivo tumor models. These results show that FAK is an important regulatory gene in melanoma. The stable FAK-knockdown melanoma cell line is an useful tool for further investigation of FAK's function in the progression of melanoma, and also an effective means of drug screening for anti-melanoma therapeutics.
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Plasmídeos / Melanoma Experimental / RNA Mensageiro / Transfecção / Regulação para Baixo / Ciclo Celular / Fase G1 / Proteína Quinase 1 Ativada por Mitógeno / RNA Interferente Pequeno Limite: Animais Idioma: Chinês Revista: Acta Pharmaceutica Sinica Ano de publicação: 2012 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Plasmídeos / Melanoma Experimental / RNA Mensageiro / Transfecção / Regulação para Baixo / Ciclo Celular / Fase G1 / Proteína Quinase 1 Ativada por Mitógeno / RNA Interferente Pequeno Limite: Animais Idioma: Chinês Revista: Acta Pharmaceutica Sinica Ano de publicação: 2012 Tipo de documento: Artigo