A study of inhibitory effect of focal related non-kinase on the migration of hepatocarcinoma cell
- VernacularTitle:黏着斑相关非激酶抑制肝癌细胞迁移及分子机制研究
- Author:
Hong GUO
;
Jia HAO
;
Xiaoyan ZHAO
- Publication Type:Journal Article
- Keywords:
focal adhesion kinase;
hepatoma carcinoma nuclear factor-kappa B;
migration;
phosphatidylinositol 3-kinase
- From:
Medical Journal of Chinese People's Liberation Army
1981;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To determine whether focal adhesion kinase (FAK) signal pathway was involved in migration of hepatocarcinoma cells by inhibiting focal adhesion kinase (FAK) phosphorylation in HepG2 cells with focal adhesion related nonkinase (FRNK). Methods The recombinant of FRNK and pEGFP-C2, an endogenous inhibitor of FAK activation,was transfected into HepG2 cells. HepG2 migration was examined by transmembrane assay. FAK and phosphatinositol 3-kinase (PI3-K) phosphorylation were detected by immunoprecipitation method. Confocal scanning microscopy was used to verify nuclear translocation of nuclear factor-kappa B (NF-?B). Results The transfection of FRNK recombinant plasmid could inhibit HepG2 migration, FAK and PI3-K phosphorylation decreased by 50.2 percent and 39.5 percent respectively. Furthermore, NF-?B translocation was down-regulated from 3.495?0.227 to 1.182?0.106. Conclusion These results suggested FAK was a main signal pathway in mediating HepG2 migration. Over expression of FRNK might inhibit signal transduction of FAK via depression of the phosphorylation of PI3-K and NF-?b activation, resulting in the decrease in migration of hepatocarcinoma cell.
