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Ginsenoside compound K induces apoptosis in nasopharyngeal carcinoma cells via activation of apoptosis-inducing factor

Carmen Ka-Man Law1, Hoi-Hin Kwok1, Po-Ying Poon1, Chi-Chiu Lau1, Zhi-Hong Jiang2, William Chi-Shing Tai3, Wendy Wen-Luan Hsiao3, Nai-Ki Mak1, Patrick Ying-Kit Yue1* and Ricky Ngok-Shun Wong1*

Author Affiliations

1 Department of Biology, Faculty of Science, Hong Kong Baptist University, Hong Kong SAR, China

2 Faculty of Chinese Medicine, Macau University of Science and Technology, Macau SAR, China

3 Center for Cancer and Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University, Kowloon, Hong Kong SAR, China

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Chinese Medicine 2014, 9:11  doi:10.1186/1749-8546-9-11

Published: 2 April 2014



Nasopharyngeal carcinoma (NPC) has a high incidence rate in Southern China. Although there are conventional therapies, the side effects and toxicities are not always tolerable for patients. Recently, the tumoricidal effect of ginsenosides on different cancer cells has been studied. This study aims to investigate the anti-cancer effect of ginsenosides on NPC cells and their underlying mechanism.


The cytotoxicity of ginsenosides on NPC cell line HK-1 was measured by MTT assay. Apoptosis was detected by propidium iodide staining followed by flow cytometry. A xenograft tumor model was established by injecting nude mice with HK-1 cells. The activation of caspases and apoptosis-inducing factor (AIF) were evaluated by Western blot analysis. Nuclear translocation of AIF was also studied by immunofluorescence staining. Mitochondrial membrane potential was measured by JC-1 dye using flow cytometry.


Four ginsenosides, 20 (S)-Rh2, compound K (CK), panaxadiol (PD) and protopanaxadiol (PPD), induced apoptotic cell death in HK-1 cells in a concentration-dependent manner. CK inhibited HK-1 xenograft tumor growth most extensively and depleted mitochondrial membrane potential depolarization and induced translocation of AIF from cytoplasm to nucleus in HK-1 cells. In addition, depletion of AIF by siRNA abolished CK-induced HK-1 cell death.


Ginsenoside CK-induced apoptosis of HK-1 cells was mediated by the mitochondrial pathway and could significantly inhibit tumor growth in vivo.