Dendrobium candidum extract inhibits proliferation and induces apoptosis of liver cancer cells by inactivating Wnt/β-catenin signaling pathway

• Published in: Biomedicine & pharmacotherapy 2019-02, Vol.110, p.371-379
• Main Authors: Guo, Zongbing, Zhou, Yanmei, Yang, Jiping, Shao, Xiaomei
• Format: Article
• Language: English
• Subjects: Dendrobium candidum; Liver cancer; Mitochondria apoptosis; Wnt/β-catenin pathway
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2018.11.149

Dendrobium candidum extract (DCE) has been reported to have anti-tumor property. However, the effect of DCE on liver cancer has not been well explored. This study was aimed to evaluate the inhibitory effect of DCE on liver cancer cells. The effect of DCE on liver cancer cells was analyzed by detecting cell viability by MTT assay, detecting colony formation ability by colony formation assay, determining apoptotic cell rate, cell cycle distribution, active caspase-3 positive cells, Ki-67 positive cells, reactive oxygen species (ROS) level, and mitochondrial transmembrane potential (MMP) by flow cytometry analysis, and analyzing changes of expressions of cell cycle-, apoptosis-, and Wnt/β-catenin pathway-related proteins by Western blot. DCE inhibited viability and promoted apoptosis of liver cancer cell lines SMMC-7721 and BEL-7404. DCE decreased colony formation, induced cell cycle arrest, and led to cell cycle-associated proteins’ abnormal expressions in SMMC-7721 and BEL-7404 cells. DCE effectively suppressed viability and proliferation of primary liver cancer cells and also induced aberrant expressions of cell cycle- and apoptosis-related proteins. After DCE treatment, ROS level was increased and MMP level was decreased. DCE inhibited β-catenin level in the nucleus and regulated downstream genes of β-catenin and further blocked Wnt/β-catenin pathway in SMMC-7721 and BEL-7404 cells as well as primary liver cancer cells. DCE suppressed liver cancer SMMC-7721 and BEL-7404 cells as well as primary liver cancer cells likely though activating mitochondria apoptosis pathway and inducing inhibition of Wnt/β-catenin pathway.