Fig. 7

Hypothetical model illustrates the effects of sCLU on AKT/GSK-3β/β-catenin Axis. In hepatocarcinogenesis, sCLU overexpression in cytoplasm leads to the phosphorylation of AKT. Subsequently, activated AKT further phosphorylates GSK-3β, which prevents β-catenin from GSK-3β-mediated phosphorylation and degradation. The accumulation of β-catenin enhances Wnt/β-catenin-mediated CSC properties of HCC cells, results in chemoresistance and metastasis, and eventually promotes the progression of HCC