Compound K-induced apoptosis of human hepatocellular carcinoma MHCC97-H cells in vitro
| Autor: | Yanlin Ming, Zheng Guohua, Qing-Xi Chen, Zhi-Zhong Zheng, Lianghua Chen, Liu Shaosong |
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| Rok vydání: | 2014 |
| Předmět: |
Cancer Research
Carcinoma Hepatocellular Ginsenosides Apoptosis Biology Pharmacology Fas ligand chemistry.chemical_compound Cell Line Tumor Humans MTT assay Cell Proliferation Membrane Potential Mitochondrial Dose-Response Relationship Drug Cell growth Liver Neoplasms General Medicine Cell cycle Molecular biology Gene Expression Regulation Neoplastic Oncology chemistry Cell culture Cancer cell Protopanaxadiol DNA Damage |
| Zdroj: | Oncology Reports. 32:325-331 |
| ISSN: | 1791-2431 1021-335X |
| DOI: | 10.3892/or.2014.3171 |
| Popis: | An intestinal bacterial metabolite of ginseng protopanaxadiol saponin, 20-O-(β-D-glucopyranosyl)-20(S)-protopanaxadiol (compound K), has been reported to induce apoptosis in a variety of cancer cells. However, the precise mechanisms induced by compound K in human hepatocellular carcinoma (HCC) cells remain unclear. In order to examine possible apoptotic mechanisms, we investigated the anticancer effect of compound K in MHCC97-H. MTT assay showed that compound K inhibited the proliferation of MHCC97-H cells with a relatively low toxicity in normal hepatoma cells. Cell cycle progression and cell staining showed an increase in apoptotic sub-G1 fraction. Treatment of MHCC97-H with compound K also induced a reduction in mitochondrial membrane potential (Δψm) and DNA damage. Further study showed that compound K upregulated Fas, FasL, Bax/Bcl-2 ratio and downregulated pro-caspase-9, pro-caspase-3 in a dose-dependent manner, and it also inhibited Akt phosphorylation. These results suggest that compound K significantly inhibits cell proliferation and induces apoptosis in MHCC97-H cells through Fas- and mitochondria-mediated caspase-dependent pathways in human HCC cells. |
| Databáze: | OpenAIRE |
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