Background: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death in the world. Paris polyphylla, also known as Chong-lou in China, is traditionally used as an anticancer medicine. Paris saponin H (Ps H) has been reported to be one potential antitumor active component from Paris polyphylla and shows cytotoxicity on tumor cells. However, the role of Ps H in HCC is not clear.
Methods: PLC/PRF/5 and Huh7 cells were exposed to Ps H. Cell viability, migration, and invasion were measured with CCK-8 assay, EMT and Transwell assay, respectively. Western blot was employed to detect the expression of cleaved caspase 3, E-cadherin, vimentin, β-catenin, p-GSK-3β and GSK-3β. Apoptosis was assessed by flow cytometry, and caspase 3 activity assay. For in vivo experiments, xenograft tumors were induced with PLC/PRF/5 cells.
Results: Ps H reduced cell viability and induced apoptosis in HCC cells in the dose-dependent manner; EMT and invasion were inhibited by Ps H. Ps H downregulated expression of β-catenin and p-GSK-3β; in addition, β-catenin silencing mediated Ps H-induced suppression of cell progression in PLC/PRF/5 cells. An administration of Ps H effectively suppressed the tumor growth in the HCC xenograft model in vivo.
Conclusion: Ps H suppresses HCC cell progression through downregulation of β-catenin in vitro, and inhibits xenograft tumor growth, suggesting Ps H is an attractive candidate for clinical therapy for HCC.
Keywords: Paris saponin H (Ps H); cell progression; hepatocellular carcinoma (HCC); β-catenin.
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