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

被引：108

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

来源：

CANCER INVESTIGATION | 2009年 / 27卷 / 07期

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

页码：723 / 733

页数：11

共 57 条

[1]

Achiwa Y, 2005, ONCOL REP, V13, P51

[2] Cell-specific regulation of apoptosis by glucocorticoids: implication to their anti-inflammatory action [J].