Zongbing Guo1, Yanmei Zhou1, Jiping Yang1, Xiaomei Shao2. 1. Department of Traditional Chinese Medicine, Jining No. 1 People's Hospital, Jining, 272100, China. 2. Department of Traditional Chinese Medicine, Jining No. 1 People's Hospital, Jining, 272100, China. Electronic address: xiaomeimei1220@sina.com.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.