他莫昔芬对ER- GPER+乳腺癌细胞上皮间质转化的影响及机制

doi:10.3969/j.issn.2095-9400.2020.09.008

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Abstract Objective: To investigate the effect of TAM on EMT in ER- GPER+ breast cancer cells and to discuss its signaling mechanism. Methods: ER- GPER+ breast cancer MDA-MB-468 cells were researched object. Cells were treated by TAM, intracellular GPER activity were inhibited by GPER specific inhibitor G15, GPER protein expression was interfered by siRNA , cell invasion ability was detected by invasion chamber experiment and western blot experiment was used to detect ERα, GPER, Vimentin, E-cadherin and N-cadherin protein expression changes. Results: TAM (5 μmol/L) could significantly enhance the invasion ability of MDA-MB-468 cells (P<0.01), and G15 (10 μmol/L) pretreatment could significantly inhibit TAM-induced cell invasion (P<0.01). GPER-siRNA could significantly interfere with the expression of GPER protein in MDA-MB-468 cells (P<0.01), and interference with GPER protein expression could effectively inhibit TAM-induced cell invasion (P<0.01). TAM treatment significantly induced up-regulation of Vimentin and N-cadherin protein expression (P<0.01) and down-regulation of E-cadherin protein expression (P<0.01). G15 pretreatment or interference with GPER protein expression could inhibit the above induction of TAM (P<0.05). Conclusion: TAM can induce EMT in ER-GPER+ breast cancer MDA-MB-468 cells, which is related to the activation of GPER.

Key words： tamoxifen G protein-coupled estrogen receptor breast carcinoma epithelial-mesenchymal transition

Received: 28 October 2019

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	WANG Shumeng
	WU Meng
	GAO Xiaodan
	LI Tingting

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https://xb.wmu.edu.cn/EN/10.3969/j.issn.2095-9400.2020.09.008 OR https://xb.wmu.edu.cn/EN/Y2020/V50/I9/728

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