Tiezhu Chen1, Juan Lin1, Daxuan Tang1, Mei Zhang1, Feiyan Wen2, Dan Xue2, Hao Zhang2. 1. Sichuan Provincial Key Laboratory of Quality and Innovation Research of Chinese Materia Medica, Sichuan Academy of Chinese Medicine Sciences Chengdu, Sichuan, China. 2. West China School of Pharmacy, Sichuan University Chengdu, Sichuan, China.
Abstract
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. IJCEP
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. IJCEP