YongHong Zhang1, Feng Wei2, Jing Zhang3, Lanxiang Hao4, Jie Jiang5, Liansheng Dang2, Dan Mei5, ShanShan Fan5, Yajin Yu5, Ling Jiang6. 1. Department of Endocrinology, Qilu Hospital, Shandong University, Jinan 250012, China; Department of Endocrinology, First Affiliated Hospital, Inner Mongolia University of Technology, Baotou 014010, China. Electronic address: zhangyonghonggogo@163.com. 2. Department of Endocrinology, First Affiliated Hospital, Inner Mongolia University of Technology, Baotou 014010, China. 3. Department of Kidney Dialysis, Heze Municipal Hospital, Heze 274000, China. 4. Department of Endocrinology, Yancheng First People's Hospital, Yancheng 224001, China. 5. Department of Endocrinology, Qilu Hospital, Shandong University, Jinan 250012, China. 6. Department of Endocrinology, Qilu Hospital, Shandong University, Jinan 250012, China. Electronic address: jiangling76@medmail.com.cn.
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.
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 humanthyroid 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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