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

The Journal of Steroid Biochemistry and Molecular Biology
Xue WangJian Huang

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.

Citations

Jun 13, 2020·International Journal of Molecular Sciences·Charlène ThiebautHélène Dumond
Apr 11, 2018·Oxidative Medicine and Cellular Longevity·Ashraf B Abdel-NaimAli M El-Halawany
Apr 30, 2019·BioMed Research International·Xiao-Jing YangZi-Jian Li
Nov 28, 2020·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Fatemeh MahboobifardMohammad H Pourgholami
Oct 29, 2021·Journal of Biomedical Nanotechnology·Jingxin FuXiangtao Wang

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