Ursolic Acid Triggers Apoptosis and Bcl-2 Downregulation in MCF-7 Breast Cancer Cells

被引:107
|
作者
Kassi, E.
Sourlingas, T. G. [2 ]
Spiliotaki, M.
Papoutsi, Z.
Pratsinis, H. [2 ]
Aligiannis, N. [3 ]
Moutsatsou, P. [1 ]
机构
[1] Univ Athens, Dept Biol Chem, Sch Med, Biol Chem Lab, GR-11527 Athens, Greece
[2] NCSR Demokritos, Inst Biol, Athens 15310, Greece
[3] Univ Athens, Dept Pharm, Lab Pharmacognosy, GR-15771 Zografos, Greece
关键词
Apoptosis; Bcl-2; protein; Breast cancer; MCF-7; cells; Ursolic acid; GLUCOCORTICOID-INDUCED APOPTOSIS; RECEPTOR TRANSLOCATION; DEPENDENT APOPTOSIS; ANTICANCER ACTIVITY; EPITHELIAL-CELLS; PROSTATE-CANCER; MAPK ACTIVATION; DNA-BINDING; KAPPA-B; AP-1;
D O I
10.1080/07357900802672712
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
In this report we determine the ability of ursolic acid (UA) to induce apoptosis and to modulate glucocorticoid receptor (GR) and Activator Protein-1 (AP-1) in MCF-7 cells. The UA-induced apoptosis (53 M), the PARP cleavage, and the decrease in Bcl-2 protein (53 M) support the notion that UA induces apoptosis through the intrinsic mitochondrial pathway. UA binds GR (relative binding affinity: 2.57) and translocates GR into nucleus, suggesting its potential as a GR modulator. UA had no effect on GRE- or TRE-driven gene expression. In summary, UA is a GR modulator and may be considered as a potential anticancer agent in breast cancer.
引用
收藏
页码:723 / 733
页数:11
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