Ginsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells

被引:198
作者
Trang Thi Mai [1 ,4 ]
Moon, JeongYong [1 ,4 ]
Song, YeonWoo [1 ,4 ]
Pham Quoc Viet [2 ,4 ]
Pham Van Phuc [2 ,4 ]
Lee, Jung Min [3 ,4 ]
Yi, Tae-Hoo [3 ,4 ]
Cho, Moonjae [4 ]
Cho, Somi Kim [1 ,5 ]
机构
[1] Jeju Natl Univ, Fac Biotechnol, Coll Appl Life Sci, Cheju 690756, South Korea
[2] Vietnam Natl Univ, Univ Sci, Lab Stem Cell Res & Applicat, Ho Chi Minh City, Vietnam
[3] Kyung Hee Univ, Coll Life Sci, Dept Oriental Med Mat & Proc, Gyeonggi 446701, South Korea
[4] Jeju Natl Univ, Sch Med, Dept Med, Cheju 690756, South Korea
[5] Jeju Natl Univ, Subtrop Hort Res Inst, Cheju 690756, South Korea
基金
新加坡国家研究基金会;
关键词
Apoptosis; Autophagy; Breast cancer stem cells; Ginsenoside F2; MYELOID-LEUKEMIA; CYCLE ARREST; P53; DEATH; IDENTIFICATION; INHIBITION; SURVIVAL; EXPRESSION; INDUCTION; RECEPTOR;
D O I
10.1016/j.canlet.2012.01.045
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Ginsenoside F2 (F2) was assessed for its antiproliferative activity against breast cancer stem cells (CSCs). F2 induced apoptosis in breast CSCs by activating the intrinsic apoptotic pathway and mitochondrial dysfunction. Concomitantly, F2 induced the formation of acidic vesicular organelles, recruitment of GFP-LC3-II to autophagosomes, and elevation of Atg-7 levels, suggesting that F2 initiates an autophagic progression in breast CSCs. Treatment with an inhibitor of autophagy enhanced F2-induced cell death. Our findings provide new insights into the anti-cancer activity of F2 and may contribute to the rational use and pharmacological study of F2. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:144 / 153
页数:10
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