The ginsenoside metabolite compound K inhibits hormone-independent breast cancer through downregulation of cyclin D1

被引:18
作者
Lee, Seung Joon [1 ,5 ]
Lee, Ji Su [2 ]
Lee, Eunjung [3 ]
Lim, Tae-Gyu [4 ]
Byun, Sanguine [2 ]
机构
[1] Seoul Natl Univ, Dept Agr Biotechnol, Seoul 08826, South Korea
[2] Incheon Natl Univ, Div Bioengn, Incheon 22012, South Korea
[3] Korea Food Res Inst, Tradit Alcohol Beverage Res Team, Wanju Gun 55365, Jeollabuk Do, South Korea
[4] Korea Food Res Inst, Wanju Gun 55365, Jeollabuk Do, South Korea
[5] CELLTRION Inc, Incheon 22014, South Korea
基金
新加坡国家研究基金会;
关键词
Compound K; Hormone-independent breast cancer; Cyclin D1; ESTROGEN-RECEPTOR; MCF-7; CELLS; EXPRESSION; GROWTH; OVEREXPRESSION; SAPONIN; TARGET; PHOSPHORYLATION; PROLIFERATION; AMPLIFICATION;
D O I
10.1016/j.jff.2018.04.050
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Various types of ginsenosides are present in ginseng and have been recognized for their health-promoting effects. Compound K (CK) is a metabolite of ginsenoside Rb1 and reportedly exerts chemotherapeutic effects against several types of cancers. However, the anti-cancer effect and the molecular mechanism of CK against hormone-independent breast cancer is unknown. Through a direct comparison, it was discovered that CK elicits the strongest anti-cancer effect against breast cancer cells when compared to other ginsenosides. CK treatment suppresses the growth of hormone-independent human breast cancer cells and induces G1 phase cell cycle arrest. CK also markedly suppresses tumor growth in a mouse xenograft model, concomitant with the suppression of cyclin D1 via protein degradation. These findings suggest that CK can be used to target hormone-independent breast cancers by inducing degradation of cyclin D1.
引用
收藏
页码:159 / 166
页数:8
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