In this study, Cav-1 overexpression promoted metastasis potential of HBV-associated HCC by stabilizing β-catenin, while CP administration induced autophagic degradation of Cav-1, activated the Akt/GSK3β-mediated proteasome degradation of β-catenin via ubiquitination activation, and subsequently attenuated the metastasis-promoting effect of Cav-1. Here, CAV1 is linked to hepatocellular carcinoma.