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J Steroid Biochem Mol Biol. 2017 Jul;171:318-327. doi: 10.1016/j.jsbmb.2017.05.009. Epub 2017 May 18.

Estrogen receptor-α36 is involved in icaritin induced growth inhibition of triple-negative breast cancer cells.

Author information

1
Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, Hubei Province 430072, PR China.
2
Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, Hubei Province 430072, PR China; College of Bioengineering, Wuhan Polytechnic, Wuhan, Hubei Province 430074, PR China.
3
Department of Pathology and Pathophysiology, School of Medicine, Jianghan University, Wuhan, Hubei Province 430056, PR China.
4
Department of Pathology and Pathophysiology, School of Medicine, Jianghan University, Wuhan, Hubei Province 430056, PR China. Electronic address: liulijiang@163.com.
5
Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, Hubei Province 430072, PR China. Electronic address: jianhuang@whu.edu.cn.

Abstract

A sub-class of ER-negative breast cancer that is negative for ER, PR and HER2 expression known as triple-negative breast cancer (TNBC) is highly malignant and lacks effective treatment. Recently, it has been reported that an isoform of estrogen receptor-alpha ER-α36 is expressed and plays a critical role in development of TNBC. ER-α36 forms a positive regulatory loop with epidermal growth factor receptor (EGFR), which promotes malignant growth of TNBC cells. Thus, ER-α36 has been proposed as an important target for development of novel drugs for TNBC. In this study, we evaluated the effects of icaritin, a prenylflavonoid derivant purified from Epimedium Genus, on growth of TNBC cells and examined the possible underlying mechanisms. Our study demonstrated that icartin decreased both ER-α36 and EGFR protein expression, and induced apoptosis in TNBC MDA-MB-231 and MDA-MB-453 cells. We also found that icaritin inhibited ER-α36-mediated MAPK/ERK pathway and cyclin D1 induction by estrogen. Our results thus indicated that icaritin has a potential to be developed into a novel therapeutic agent for human TNBC.

KEYWORDS:

Apoptosis; ER-α36; Growth inhibition; Icaritin; Triple-negative breast cancer

PMID:
28529129
DOI:
10.1016/j.jsbmb.2017.05.009
[Indexed for MEDLINE]

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