Caudatin Inhibits Cell Proliferation and Migration Via Apoptosis in Human Hepatocellular Carcinoma Cells

The aim of this study was to investigate the impact of caudatin on the biological function of hepatocellular carcinoma cells in vitro, as well as to further explore its effects and underlying mechanism. The effect of caudatin on the proliferation of HepG2 and Huh7 cells was evaluated using a CCK-8 assay. Flow cytometry and scratch test were employed to assess the potential of caudatin to induce apoptosis and inhibit cell migration. Caudatin significantly suppressed the in vitro proliferation of HepG2 and Huh7 cells in a dose-dependent manner. The IC50 values for caudatin against HepG2 and Huh7 cells were 10.1 mu M and 7.6 mu M, respectively. Furthermore, it exhibited inhibitory effects on the scratch wound healing rate of both HepG2 and Huh7 cells, as well as induced apoptosis. Additionally, mRNA expression analysis revealed that caudatin significantly inhibited the expression levels of GSK3 beta, uPA, MMP9, PR, PlGF, SyK, RAR beta, and JAK2 proteins. Molecular docking studies suggested strong binding affinities between caudatin and uPA, MMP9, and JAK2 through hydrogen bond and hydrophobic interactions. Furthermore, caudatin exhibited rapid elimination from the body, suggesting its classification as a drug with fast clearance rates and minimizing the risk of accumulation-induced toxicity.