Horm Metab Res 2013; 45(08): 593-598
DOI: 10.1055/s-0033-1341510
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Calycosin Induces Apoptosis by Upregulation of RASD1 in Human Breast Cancer Cells MCF-7

J. Tian
1   Department of physiology, Guilin Medical University, Guilin, China
,
Y. X. Duan
2   Department of Obstetrics and Gynecology, Third Affiliated Hospital of Xinxiang Medical College, Xinxiang, China
,
C. Y. Bei
3   Department of Limbs Trauma Orthopedics, Affiliated Hospital of Guilin Medical University, Guilin, China
,
J. Chen
4   School of Basic Medical Sciences, Guilin Medical University, Guangxi, Guilin, China
› Author Affiliations
Further Information

Publication History

received 23 January 2013

accepted 11 March 2013

Publication Date:
22 April 2013 (online)

Abstract

Breast cancer is a leading cause of cancer death among women, and the failure of normal apoptosis has been proved in the development of breast cancer. The phytoestrogen, calycosin, is extracted from Chinese medical herb Radix astragali. We recently reported that calycosin successfully stimulated proliferation of ER-positive MCF-7 human breast cancer cells at low concentration. In the present study, we assessed the proapoptotic function of calycosin in MCF-7 cells at high concentration in vitro, as well as the possible mechanism of its effect. MCF-7 cells were treated with different concentrations of calycosin, and then detected by MTT assay for cellular viability, Hoechst assay, and flow cytometry for apoptosis. RASD1 is identified as a Ras-family member and a regulator in MAPK-mediated cascade leading to cell proliferation or apoptosis. To provide insight into the functions of RASD1 signaling pathway in calycosin-induced apoptosis, the expression of Bcl-2, Bax, and RASD1 in calycosin-treated cells were determined by Western blot assay. The results showed that high concentrations of calycosin significantly suppressed the proliferation of MCF-7 cells and promoted cell apoptosis. Moreover, compared with control group, the expression of Bcl-2 decreased with calycosin in MCF-7 cells, while Bax increased, which was significantly correlated with elevated expression of RASD1. Together, we present evidence that at relatively high concentration calycosin triggered cell apoptosis through the mitochondrial apoptotic pathway by upregulating RASD1. And for the first time, this study revealed that calycosin may have potential as a therapeutic agent for the treatment of breast cancer.

 
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