Daphnetin inhibits the survival of hepatocellular carcinoma cells through regulating Wnt/β‐catenin signaling pathway
LIU Chaohui, Jiansheng Pan, Hongyu Liu, Rongkai Lin, Yijie Chen, Chenghua Zhang
Abstract
Evidence has demonstrated that Daphnetin has antiangiogenesis activity, indicating it might be a new multi-targeted medication for cancer therapy. Here, we aimed to reveal Daphnetin role in hepatocellular carcinoma (HCC) progression and the underlying mechanism. Huh7 and SK-HEP-1, two human HCC cell lines were used in this study. MTT （3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide）, colony formation, flow cytometry, and tumor-bearing experiments were applied to evaluate the effects of different concentrations of Daphnetin on cell viability, apoptosis, cell cycle, and in vivo tumor formation, respectively. Real-time PCR （Polymerase Chain Reaction）and western blotting were applied to measure the mRNA and protein levels of β-catenin. We observed that Daphnetin inhibited cell viability and tumorigenesis, promoted cell apoptosis, and induced a G1 phase arrest in a dose-dependent manner in both Huh7 and SK-HEP-1 cells, which were rescued by SKL2001, an activator of the Wnt/β-catenin signaling. Taken together, this study reveals that Daphnetin exerts an antitumor role in HCC through the inactivation of Wnt/β-catenin signaling.