Cellular and molecular mechanisms of silibinin induces cell-cycle arrest and apoptosis on HeLa cells

被引:29
作者
Zhang, Y. [1 ,2 ]
Ge, Y. [1 ,2 ]
Chen, Y. [3 ]
Li, Q. [1 ]
Chen, J. [4 ]
Dong, Y. [4 ]
Shi, W. [1 ]
机构
[1] Jilin Univ, Key Lab Mol Enzymol & Engn, Minist Educ, Life Sci Coll, Changchun 130012, Jilin, Peoples R China
[2] Jilin Inst Chem Technol, Coll Environm & Biol Engn, Jilin, Peoples R China
[3] Jilin Univ, Coll Pharm, Ctr Combinatorial Chem & Drug Discovery, Changchun 130012, Jilin, Peoples R China
[4] Jiangsu Univ, Sch Pharm, Zhenjiang, Jiangsu, Peoples R China
关键词
cervical cancer; silibinin; cell cycle arrest; apoptosis; mechanism; DEPENDENT KINASE INHIBITORS; ANTICANCER THERAPY; CANCER; CARCINOMA; PROLIFERATION; CHEMOTHERAPY; REGULATORS; INDUCTION; SILYMARIN; PATHWAYS;
D O I
10.1002/cbf.1842
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Silibinin, an effective anti-cancer and chemopreventive agent in various epithelial cancer models, has been reported to inhibit cancer cell growth through mitogenic signalling pathways including cervical cancer. However, the underlying mechanisms are still not well elucidated. Here, we assessed the effect of silibinin on human cervical carcinoma cell cycle modulation, apoptosis induction and associated molecular alterations by employing HeLa cell line. Silibinin treatment of HeLa cells resulted in a G2 arrest and induced a decrease in cyclin-dependent kinases involved in both G1 and G2 progression. In addition, silibinin showed a dose-dependent and a time-dependent apoptotic death in HeLa cells in both the mitochondrial pathway and the death receptor-mediated pathway, providing a strong rationale for future studies evaluating preventive and/or intervention strategies for silibinin in cervical cancer pre-clinical models. Copyright (C) 2011 John Wiley & Sons, Ltd.
引用
收藏
页码:243 / 248
页数:6
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