Aim: To understand the role of P120ctn in E-cadherin-mediated cell-cell adhesion and signaling as well as in hepatoma cell biological function.
Methods: We stably overexpressed p120ctn isoform 3A in BEL-7404 human hepatoma cells and studied the effect of p120ctn on beta-catenin and E-cadherin binding as well as p120ctn and beta-catenin subcellular localization using immunoprecipitation, Western blotting and confocal microscopy. We also investigated the inhibitory effect of p120ctn transfection on the expression of apoptotic protein survivin survivin and cell cycle regulator cyclin D1 in the cells.
Objective: To investigate the effect of catenin p120 (p120ctn) translocation on the malignant features of hepatocellular carcinoma and its interrelation with beta-catenin in E-cadherin-mediated cell signaling.
Methods: Expression and translocation of p120ctn, tyrosine phosphorylation, and its binding capacity to E-cadherin were detected by DNA transfection, immunoblotting and immunoprecipitation. Cellular localization of p120ctn and beta-catenin was detected by immunofluorescent microscopy.
Objective: In hepatocellular carcinoma cells, the tyrosine phosphorylation of p120(ctn) was stimulated by epidermal growth factor (EGF) to investigate the relationship between the tyrosine phosphorylation of p120(ctn) and the translocation of p120(ctn), also the relationship between the tyrosine phosphorylation of p120(ctn) and the biological behaviour of hepatocellular carcinoma cells. The role of p120(ctn) in the cell adhesion and signaling of hepatocellular carcinoma is to be investigated.
Methods: In BEL-7404 human hepatocellular carcinoma cells, the tyrosine phosphotyrosine of p120(ctn) stimulated by EGF were detected by immunoprecipitation (IP) and Immunoblotting (IB).