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Ji-Youn Kim,Ho-Gyu Choi,Hae-Miru Lee,Geum-A Lee,Kyung-A Hwang,Kyung-Chul Choi.Journal of Biomedical Research,2017,31(4):358-369
Effects of bisphenol compounds on the growth and epithelial mesenchymal transition of MCF-7 CV human breast cancer cells
Received:December 10, 2016  Revised:January 19, 2017
DOI10.7555/JBR.31.20160162
Keywordshuman breast cancer cells, endocrine disrupting chemicals, bisphenol-A, bisphenol-S, bisphenol-F,
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Ji-Youn Kim Laboratory of Biochemistry and Immunology, Veterinary Medical Center and College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, 28644 Republic of Korea.
Ho-Gyu Choi Laboratory of Biochemistry and Immunology, Veterinary Medical Center and College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, 28644 Republic of Korea.
Hae-Miru Lee Laboratory of Biochemistry and Immunology, Veterinary Medical Center and College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, 28644 Republic of Korea.
Geum-A Lee Laboratory of Biochemistry and Immunology, Veterinary Medical Center and College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, 28644 Republic of Korea.
Kyung-A Hwang Laboratory of Biochemistry and Immunology, Veterinary Medical Center and College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, 28644 Republic of Korea.
Kyung-Chul Choi Laboratory of Biochemistry and Immunology, Veterinary Medical Center and College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, 28644 Republic of Korea.
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Abstract
      Bisphenol-A (BPA) has been considered as an endocrine disrupting chemical (EDC) because it can exert estrogenic properties. For bisphenol-S (BPS) and bisphenol-F (BPF) that are BPA analogs and substitutes, their risk to estrogendependent cancer has been reported rarely compared with the numerous cases of BPA. In this study, we examined whether BPA, BPS, and BPF can lead to the proliferation, migration, and epithelial mesenchymal transition (EMT) of MCF-7 clonal variant (MCF-7 CV) breast cancer cells expressing estrogen receptors (ERs). In a cell viability assay, BPA, BPS, and BPF significantly increased proliferation of MCF-7 CV cells compared to control (DMSO) as did 17β-estradiol (E2). In Western blotting assay, BPA, BPS, and BPF enhanced the protein expression of cell cycle progression genes such as cyclin D1 and E1. In addition, MCF-7 CV cells lost cell to cell contacts and acquired fibroblast-like morphology by the treatment of BPA, BPS, or BPF for 24 hours. In cell migration assay, BPA, BPS, and BPF accelerated the migration capability of MCF-7 CV cells as did E2. In relation with the EMT process, BPA, BPS, and BPF increased the protein expression of N-cadherin, while they decreased the protein expression of Ecadherin. When BPA, BPS, and BPF were co-treated with ICI 182,780, an ER antagonist, proliferation effects were reversed, the expression of cyclin D1 and cyclin E1 was downregulated, and the altered cell migration and expression of N-cadherin and E-cadherin by BPA, BPS, and BPF were restored to the control level. Thus, these results imply that BPS and BPF also have the risk of breast cancer progression as much as BPA in the induction of proliferation and migration of MCF-7 CV cells by regulating the protein expression of cell cycle-related genes and EMT markers via the ER-dependent pathway.
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