Abstract: Objective To investigate the effects of aucubin (AU) on the proliferation, apoptosis, and cell cycle of human liver cancer cells line HepG2 and its mechanism of action. Methods HepG2 cells were cultured in vitro, CCK-8 method was applied to screen the optimal dosage concentration of AU. HepG2 cells were randomly grouped into a control group, an AU 12.5 mg/L group (AU L group), an AU 62.5 mg/L group (AU H group), and an AU H+Akt pathway agonist (SC79) group(AU H+SC79 group). The cell proliferation was observed in each group; 5-Ethynyl-2′-deoxyuridine (EDU) method was applied to detect cell proliferation; Flow cytometry was applied to detect cell apoptosis and cell cycle; Western blot was applied to detect the expression levels of phosphorylated protein kinase B (p-Akt), Akt, p-MDM2, MDM2, p-p53, and p53 proteins. Results AU concentrations of 12.5 and 62.5 mg/L were selected for subsequent experiments.Compared with 0 mg/L AU, the proliferation of 12.5 and 62.5 mg/L AU cells was obviously reduced (P＜0.05);Compared with the control group, the number of suspended and exfoliated cells in the AU L and AU H groups gradually increased. Cells shrunk and became round. The proportion of G0/G1 phase cells, the proportion of EDU positive staining cells increased and the expression level of p-Akt/Akt and p-MDM2/MDM2 proteins decreased. The proportions of S and G2/M phase cells, the rate of cell apoptosis, and the expression level of p-p53/p53 protein all increased (P＜0.05). Compared with the AU H group, the above changes in the AU H+SC79 group were recovered(P＜0.05). After AU treatment, the tumor volume and weight of transplanted nude mice decreased. Conclusions AU may inhibit the proliferation of liver cancer cells, induce cell cycle arrest and apoptosis by regulating the Akt/MDM2/p53 signaling pathway.

Key words: aucubin, liver cancer cell, proliferation, apoptosis, cell cycle