Inhibition of JNK1 expression decreases migration and invasion of mouse hepatocellular carcinoma cell line in vitro.
Med Oncol
; 28(4): 966-72, 2011 Dec.
Article
em En
| MEDLINE
| ID: mdl-20490718
ABSTRACT
c-Jun N-terminal kinase (JNK) is located in focal adhesion plaque (FAP). JNK is necessary to growth, morphogenesis, and differentiation of cells; especially JNK1 has a close relation with tumors. In this study, we silenced JNK1 by using short hairpin RNA (shRNA) and examined the effect on migration and invasion of mouse hepatocellular carcinoma (HCC) cell line Hca-F in vitro. Three shRNA expression vectors (JNK1shRNA-1, JNK1shRNA-2, and JNK1shRNA-3) were constructed and transfected to Hca-F cells stably. The most effective shRNA was selected by detecting the expression levels of mRNA and protein. Transwell assay was performed to detect the ability of migration and invasion of cells. A negative control sequence (JNK1shRNA control) and non-transfected normal Hca-F cells were treated as control groups. The "Results" showed that the expression vectors of pSilencer-JNK1shRNA were constructed and transfected to Hca-F cells successfully. The most effective shRNA was JNK1shRNA-2. The expressions of mRNA and protein of JNK1 in Hca-F cells after transfection of JNK1shRNA-2 were decreased significantly compared with the other groups (all, P<0.01; all, P<0.05). The ability of migration and invasion was decreased after down-regulation of JNK1 expression (all, P<0.05). These results suggest that the inhibition of JNK1 expression can decrease ability of migration and invasion of mouse hepatocellular carcinoma cell line in vitro. JNK1 plays an important role in lymphatic metastasis of HCC. It may be a new target for gene therapy of lymphatic metastasis of HCC.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Carcinoma Hepatocelular
/
Proteína Quinase 8 Ativada por Mitógeno
/
Neoplasias Hepáticas
Limite:
Animals
Idioma:
En
Revista:
Med Oncol
Assunto da revista:
NEOPLASIAS
Ano de publicação:
2011
Tipo de documento:
Article
País de afiliação:
China