In conclusion, our study demonstrated that CPC induced apoptosis and inhibited EMT by regulating the expression of apoptosis-related genes (p53, Bax, Bcl-XL, etc.)and EMT-related genes (Slug, E-cadherin, N-cadherin, and Vimentin) in a dose-dependent manner, thereby inhibiting the proliferation, invasion, and metastasis of HCC cells in vivo and in vitro, suggesting that CPC is a potential agent for HCC (Fig 6F). This evidence concerns the gene BCL2L1 and hepatocellular carcinoma.