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Bisphenol A and estrogen induce proliferation of human thyroid tumor cells via an estrogen-receptor-dependent pathway.

Bisphenol A and estrogen induce proliferation of human thyroid tumor cells via an estrogen-receptor-dependent pathway.
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Zhang Y, Wei F, Zhang J, Hao L, Jiang J, Dang L, Mei D, Fan S, Yu Y, Jiang L,


Zhang Y, Wei F, Zhang J, Hao L, Jiang J, Dang L, Mei D, Fan S, Yu Y, Jiang L, (click to view)

Zhang Y, Wei F, Zhang J, Hao L, Jiang J, Dang L, Mei D, Fan S, Yu Y, Jiang L,

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Archives of biochemistry and biophysics 2017 09 04633() 29-39 pii 10.1016/j.abb.2017.09.002

Abstract
OBJECTIVE
To determine the relationship between papillary thyroid carcinoma and environmental exposure to bisphenol A (BPA) or 17-β estrogen (E2) by assessing the effects of these compounds on estrogen receptor expression and AKT/mTOR signaling.

METHODS
The effects of low levels of BPA (1mM-10nM) and 17β-estradiol (E2, 0.1mM-1nM) on ER expression and cellular proliferation were determined in human thyroid papillary cancer BHP10-3 cells. Protein and mRNA levels of estrogen nuclear receptors (ERα/ERβ) and membrane receptors (GPR30) were determined by immunofluorescence assay, Western blotting, and RT-PCR, respectively, and proliferation was assessed by CCK-8 assay.

RESULTS
The proliferative effects of BPA and E2 were both concentration- and time-dependent. Expression of ERα/ERβ and GPR30 were enhanced by BPA and E2. BPA and E2 could quickly phosphorylate AKT/mTOR. Moreover, ICI suppressed ERα expression and activated GPR30 as did G-1. G-15 reversed the effects of E2 on GPR30 and AKT/mTOR, but did not alter the effect of BPA.

CONCLUSIONS
BPA influences thyroid cancer proliferation by regulating expression of ERs and GPR30, a mechanism that differs from E2. In addition, ICI and G-15 may have the potential to be used as anti-thyroid cancer agents.

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