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Endocrine Abstracts (2015) 37 OC2.5 | DOI: 10.1530/endoabs.37.OC2.5

ECE2015 Oral Communications Reproduction (5 abstracts)

Bisphenol A-induced epithelial-mesenchymal transition was reversed with a phytoestrogen, genistein via oestrogen receptor and downregulation of transforming growth factor-beta signalling pathway

Ye-Seul Kim , Kyung-A Hwang & Kyung-Chul Choi


Laboratory of Biochemistry and Immunology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea.


Epithelial–mesenchymal transition (EMT) is an important process appeared in tumour migration or progression, which is activated by 17β-estradiol (E2). As a typical endocrine disrupting chemical (EDC), bisphenol A (BPA) has a potential to promote EMT and migration of oestrogen responsive cancers. On the contrary, genistein (GEN) as a phytoestrogen is known to have chemopreventive effects in diverse cancers. In the present study, the effects of BPA and GEN on EMT and migration of BG-1 ovarian cancer cells and the underlying mechanism were investigated. ICI 182,780, an oestrogen receptor (ER) antagonist, was co-treated with E2 or BPA to BG-1 cells to identify the relevance of ER signalling in EMT and migration. As results, E2 and BPA upregulated the protein expression of vimentin, cathepsin D, and MMP-2, but downregulated the protein expression of E-cadherin via ER signalling, suggesting that E2 and BPA promoted EMT and cell migration related gene expressions. However, the increased protein expression of Vimentin, Cathepsin D, and MMP-2 by E2 or BPA was reduced by the co-treatment of GEN. In a scratch assay, the migration capability of BG-1 cells was enhanced by E2 and BPA via ER signalling pathway, but reversed by the co-treatment of GEN. In the protein expression of SnoN and Smad3, E2 and BPA upregulated SnoN, a negative regulator of TGF-β signalling, and downregulated Smad3, a transcription factor in the downstream pathway of TGF-β signalling, suggesting that E2 and BPA simultaneously lead the downregulation of TGF-β signalling in the process of induction of EMT and migration of BG-1 cells via ER signalling. On the other hand, the co-treatment of GEN reversed the downregulation of TGF-β signalling by E2 and BPA. Taken together, GEN suppressed EMT and migration capacities of BG-1 ovarian cancer cells enhanced by E2 and BPA via ER signalling and the downregulation of TGF-β signalling.

Disclosure: This work was also supported by a grant from the Next-Generation BioGreen 21 Program (no. PJ009599), Rural Development Administration, Republic of Korea.

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