Role And Mechanism Of Estrogen Receptor Alpha 46 In Papillary Thyroid Carcinoma Cells

Objection: To investigate the role and the relevant mechanism of ER?46 in human thyroid papillary carcinoma cells.Methods: Expression of ER?46/ER?66 in thyroid papillary carcinoma BCPAP cells and normal thyroid Nthy-ori3-1 cells were detected by Western blot.Eukaryotic expression plasmid vector of ER?46 was constructed and transfected into BCPAP cells,and the levels of ER?46/ER?66 were analyzed by Western blot analysis.RNA extraction,reverse transcription and real-time quantitative polymerase chain were used reaction to detect the expression of c-fos and cyclin D1 mRNA in cells.The cell cycle distribution was assessed by flow cytometry.Cell counting method was used to detect the proliferation of BCPAP cells with over expression of ER?46.Cell apoptosis was detected by flow cytometry.Expression of miRNA21 was detected by RT-PCR.Western blot was used to detect the expression of PDCD4 and PTEN.Result: The ratio of ER?46/ER?66 was downregulated in thyroid papillary carcinoma BCPAP cells than when compared with normal thyroid cells down(P ? 0.05).Overexpression of ER?46 leaded to the upregulation of the ratio of ER?46/ER?66 in BCPAP cells.Overexpression of ER?46 inhibited the expression of c-fos and Cyclin D1 mRNA in BCPAP cells induced by estrogen(P?0.05).Overexpression of ER?46 inhibited cell cycle transition induced by estrogen in BCPAP cells(P?0.05).Overexpression of ER?46 inhibited the proliferation induced by estrogen in BCPAP cells(P?0.05).The expression of miRNA21 was decreased in ER?46 overexpressing cells(P < 0.05)and estrogen induced the decrease of miRNA21 expression(P < 0.05).The expression of PDCD4 and PTEN was significantly increased(P < 0.05)in BCPAP cells with overexpression of ER?46.Conclusion: Overexpression of ER?46 inhibits proliferation and promotes apoptosis of papillary thyroid carcinoma cells by up-regulating the ratio of ER?46/ER?66.