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KMID : 0545120150250071170
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Journal of Microbiology and Biotechnology
2015 Volume.25 No. 7 p.1170 ~ p.1176
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A Bacterial Metabolite, Compound K, Induces Programmed Necrosis in MCF-7 Cells via GSK3β
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Kwak Chae-Won
Son Young-Min
Gu Min-Jeong
Kim Gi-Rak
Lee In-Kyu
Kye Yoon-Chul
Kim Han-Wool
Song Ki-Duk
Chu Hyuk
Park Byung-Chul
Lee Hak-Kyo
Yang Deok-Chun
Jonathan Sprent
Yun Cheol-Heui
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Abstract
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Ginsenosides, the major active component of ginseng, are traditionally used to treat various diseases, including cancer, inflammation, and obesity. Among these, compound K (CK), an intestinal bacterial metabolite of the ginsenosides Rb1, Rb2, and Rc from Bacteroides JY-6, is reported to inhibit cancer cell growth by inducing cell-cycle arrest or cell death, including apoptosis and necrosis. However, the precise effect of CK on breast cancer cells remains unclear. MCF-7 cells were treated with CK (0-70 μM) for 24 or 48 h. Cell proliferation and death were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assays, respectively. Changes in downstream signaling molecules involved in cell death, including glycogen synthase kinase 3β (GSK3β), GSK3β, β-catenin, and cyclin D1, were analyzed by western blot assay. To block GSK3β signaling, MCF-7 cells were pretreated with GSK3β inhibitors 1 h prior to CK treatment. Cell death and the expression of β-catenin and cyclin D1 were then examined. CK dose- and time-dependently inhibited MCF-7 cell proliferation. Interestingly, CK induced programmed necrosis, but not apoptosis, via the GSK3β signaling pathway in MCF-7 cells. CK inhibited GSK3β phosphorylation, thereby suppressing the expression of β-catenin and cyclin D1. Our results suggest that CK induces programmed necrosis in MCF-7 breast cancer cells via the GSK3β signaling pathway.
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KEYWORD
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compound K, ginsenoside, programmed necrosis, breast cancer cells, MCF-7, GSK3β
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