Effects of an estrogen receptor antagonist on proliferation, prolactin secretion and growth factor expression in the MMQ pituitary prolactinoma cell line

Effects of an estrogen receptor antagonist on proliferation, prolactin secretion and growth factor expression in the MMQ pituitary prolactinoma cell line
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雌激素受体拮抗剂对 MMQ 垂体催乳素瘤细胞系增殖、催乳素分泌和生长因子表达的影响。

DOI:
10.1016/j.jocn.2011.06.013
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发表时间:
2011-12-01
影响因子:
2
通讯作者:
Zhang, Yazhuo
Zhang, Yazhuo
中科院分区:
医学4区
文献类型:
--
作者:
Leng, Lige;Zhang, Yazhuo

文献摘要

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本研究的目的是探讨MMQ垂体泌乳素瘤细胞中雌激素受体α(ER α)的功能作用,在没有雌激素的情况下,增殖,泌乳素(PRL)分泌,和生长因子的表达。用ER α拮抗剂氟维司群处理MMQ细胞,然后使用MTS和酶联免疫吸附测定法测量增殖和PRL分泌。采用定量聚合酶链反应和蛋白质印迹法检测ER α、血管内皮生长因子(VEGF)、基质金属蛋白酶-9(MMP-9)和B细胞白血病/淋巴瘤-2(BCL-2)水平。氟维司群是ER α表达的强效抑制剂,可显著抑制细胞增殖(高达57.6 +/- 2.2%)和PRL分泌(高达81.0%)。氟维司群还显著改变了VEGF、MMP-9和BCL-2的表达水平。我们的结论是,ER α在垂体泌乳素瘤中起着重要的功能作用,也参与了特定生长因子的表达,即使在没有雌激素的情况下。氟维司群治疗可能是此类肿瘤的有效疗法。(C)2011爱思唯尔有限公司保留所有权利。
The aim of this study was to investigate the functional role of estrogen receptor alpha (ER alpha) in MMQ pituitary prolactinoma cells in the absence of estrogen with respect to proliferation, prolactin (PRL) secretion, and expression of growth factors. MMQ cells were treated with the ERa antagonist fulvestrant, then proliferation and PRL secretion were measured using MTS and enzyme-linked immunosorbent assays. Levels of ER alpha, vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9) and B cell leukemia/lymphoma-2 (BCL-2) were measured using quantitative polymerase chain reaction and western blot analysis. Fulvestrant acted as a potent inhibitor of ER alpha expression, and significantly inhibited cell proliferation (by up to 57.6 +/- 2.2%) and PRL secretion (by up to 81.0%). Fulvestrant also significantly altered the expression levels of VEGF, MMP-9 and BCL-2. We conclude that ER alpha plays an important functional role in pituitary prolactinomas and is also involved in the expression of particular growth factors, even in the absence of estrogen. Fulvestrant treatment may be an effective therapy for such tumors. (C) 2011 Elsevier Ltd. All rights reserved.