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. 2017 Oct 31;8(61):104247–104257. doi: 10.18632/oncotarget.22200

Figure 4. bFGF induced EMT in HepG2 and Huh7 cells by enhancing the stability of Twist1 through the AKT/GSK-3β signalling pathway.

Figure 4

(A) Twist1 expression was detected by western blotting after bFGF treatment or not. (B) After HepG2 and Huh7 cells were treated with MG132 or a combination of MG132 and bFGF, ubiquitin was immunoprecipitated by Twist1, and its expression was detected by western blotting. (C) After treatment with bFGF or bFGF and LY294002 (20 ng/ml), p-AKT, AKT, p-GSK3β, GSK-3β and Twist1 expression was evaluated by western blotting. (D) After treating HepG2 and Huh7 cells with bFGF for 48 h, GSK-3β was immunoprecipitated by Twist1, and its expression was detected by western blotting. (E) After treatment with bFGF or bFGF and metformin together, p-AKT, AKT, p-GSK3β, GSK-3β and Twist1 expression was assessed by western blotting.