Albiflorin enhances the antitumor effects of propofol in hepatocellular carcinoma cells by inhibiting the Wnt/β-catenin signaling activation.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common types of primary liver cancer worldwide. It is characterized by high heterogeneity and poor prognosis, and current treatment outcomes remain limited. Studies have shown that propofol possesses certain anticancer properties. However, the combined effects of albiflorin and the underlying mechanisms remain unclear. This study aimed to evaluate the anticancer activity of albiflorin in HCC, further investigate the combined effects and underlying mechanism of albiflorin and propofol. METHODS: Huh-7 cells were treated with different concentrations of albiflorin (0, 25, 50, and 100 μg/mL) and propofol (0, 30, 60, and 120 μM), either alone or in combination. The effects on cell proliferation, apoptosis, migration, and invasion were evaluated. Cell proliferation was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis and epithelial-mesenchymal transition (EMT) were measured by flow cytometry and western blotting, and cell migration and invasion were evaluated using Transwell assays. Additionally, the expression of key Wnt/β-catenin signaling molecules was analyzed by western blotting and reverse transcription-quantitative polymerase chain reaction to explore potential mechanisms. RESULTS: Both albiflorin and propofol alone inhibited the proliferation, migration, invasion, and EMT of Huh-7 cells in a dose-dependent manner and promoted apoptosis. The combination of albiflorin and propofol effectively enhanced the inhibitory effects of propofol on HCC cells. Mechanistic studies revealed that the combined treatment significantly downregulated the expression of Wnt3a and β-catenin, suggesting that the antitumor effects may be mediated through the suppression of the Wnt/β-catenin signaling pathway. CONCLUSIONS: Albiflorin and propofol exert synergistic inhibitory effects on HCC cell proliferation, migration, invasion, and EMT while promoting apoptosis. These effects are likely associated with suppression of Wnt/β-catenin signaling. This study provides new experimental evidence supporting the development of multitargeted combination therapies and identifies potential molecular targets for comprehensive HCC treatment.