Fig. 7From: Cx32 exerts anti-apoptotic and pro-tumor effects via the epidermal growth factor receptor pathway in hepatocellular carcinomaCx32 upregulates the expression and activation of EGFR by binding with Src. a and b. In HCC cell lines, silencing or overexpressing Cx32 caused Src downregulation or upregulation, respectively. **, P < 0.01 versus HepG2 NC (a) or SMMC-7721 Vector (b). c. Silencing Cx32 by siCx32 transfection caused a decrease in the EGFR and Src mRNA levels in HepG2 cells, as determined by qPCR. GAPDH was used as the loading control. **, P < 0.01 versus NC. d. Overexpression of Cx32 in SMMC-7721 cells upregulated the mRNA levels of Cx32 (left panel), EGFR and Src (right panel), as determined by qPCR. GAPDH was used as the loading control. **, P < 0.01 versus Vector. e. The decrease in the levels of EGFR, p-EGFR and Src mediated by siCx32 was reversed by cotransfection of the Src overexpression vector in HepG2 cells. **, P < 0.01 versus NC. f. The increase in the levels of EGFR, p-EGFR and Src induced by Cx32 overexpression was rescued by cotransfection of siSrc in SMMC-7721 cells. **, P < 0.01 versus Vector. g and h. Cx32, p-EGFR and Src interacted with each other, as detected by CO-IP experiments in HepG2 cells (g) and SMMC-7721 cells (h). Lysate supernatants incubated without antibody, termed Input, were used as the positive control, and proteins precipitated by IgG were used as the negative controlBack to article page