Research Papers:
Cyanidin-3-o-glucoside directly binds to ERα36 and inhibits EGFR-positive triple-negative breast cancer
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Abstract
Li Wang1,*, Haifeng Li1,*, Shiping Yang1, Wenqiang Ma1, Mei Liu2, Shichao Guo1, Jun Zhan3, Hongquan Zhang3, Suk Ying Tsang4, Ziding Zhang1, Zhaoyi Wang5, Xiru Li2, Yang-Dong Guo1, Xiangdong Li1
1State Key Laboratory of the Agro-Biotechnology, College of Horticultural Science, China Agricultural University, Beijing, China
2Department of General Surgery, The 301th Hospital of PLA, Beijing, China
3Key Laboratory of Carcinogenesis and Translational Research, Ministry of Education, State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, China
4School of Life Sciences and State Key Laboratory of Agro-Biotechnology, Chinese University of Hong Kong, Hong Kong, China
5Beijing Shenogen Pharma Group, Beijing, China
*These authors have contributed equally to this work
Correspondence to:
Yang-Dong Guo, email: [email protected]
Xiru Li, email: [email protected]
Zhaoyi Wang, email: [email protected]
Xiangdong Li, email: [email protected]
Keywords: Cy-3-glu, ERα36, EGFR, triple-negative breast cancer, apoptosis
Received: December 03, 2015 Accepted: September 02, 2016 Published: September 15, 2016
ABSTRACT
Anthocyanins have been shown to inhibit the growth and metastatic potential of breast cancer (BC) cells. However, the effects of individual anthocyanins on triple-negative breast cancer (TNBC) have not yet been studied. In this study, we found that cyanidin-3-o-glucoside (Cy-3-glu) preferentially promotes the apoptosis of TNBC cells, which co-express the estrogen receptor alpha 36 (ERα36) and the epidermal growth factor receptor (EGFR). We demonstrated that Cy-3-glu directly binds to the ligand-binding domain (LBD) of ERα36, inhibits EGFR/AKT signaling, and promotes EGFR degradation. We also confirmed the therapeutic efficacy of Cy-3-glu on TNBC in the xenograft mouse model. Our data indicates that Cy-3-glu could be a novel preventive/therapeutic agent against the TNBC co-expressed ERα36/EGFR.
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