Inhibition of MCF-7 breast cancer cell proliferation by MCF-10A breast epithelial cells in coculture
Inhibition of MCF-7 breast cancer cell proliferation by MCF-10A breast epithelial cells in coculture
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DOI：
10.1016/j.cellbi.2005.11.006
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发表时间：
2006-03-01
影响因子：
3.9
通讯作者：
Spink, DC
中科院分区：
文献类型：
--
作者：
Spink, BC;Cole, RW;Spink, DC
建立了一种共培养系统，以研究稳定表达绿色荧光蛋白（MCF-7-GFP）的MCF-10 A乳腺上皮细胞和MCF-7乳腺癌细胞之间的相互作用。用该MCF-10A/MCF-7-GFP共培养系统油微量滴定板和在重构基底膜（Matrigel）上的研究揭示了MCF-7-GFP细胞增殖的旁分泌抑制。表皮生长因子在单一培养物中适度增强MCF-7-GFP并显著增加MCF-10A细胞增殖，在MCF-10A/MCF-7-GFP共培养物中极大地抑制MCF-7-GFP细胞增殖。在单一培养物中刺激MCF-7-GFP但不刺激MCF-10A细胞增殖的17 β-雌二醇在MCF-10A/MCF-7-GFP共培养物中抑制MCF-7-GFP细胞增殖，该作用被抗雌激素ICI 182，780阻断。在Matrigel上，在真实的时间内观察到复杂的MCF-10 A/MCF-7-GFP细胞相互作用，导致腺泡样结构的形成。这些结果表明正常上皮细胞在抑制肿瘤细胞增殖中的作用，并证明了这种共培养系统作为乳腺癌早期旁分泌控制模型的实用性。(C)2006年国际细胞生物学联合会。由爱思唯尔有限公司出版。保留所有权利。
A coculture system was developed to investigate the interactions between MCF-10A breast epithelial cells and MCF-7 breast cancer cells stably expressing the green fluorescent protein (MCF-7-GFP). Studies with this MCF-10A/MCF-7-GFP coculture system oil microtiter plates and on reconstituted basement membrane (Matrigel), revealed paracrine inhibition of MCF-7-GFP cell proliferation. Epidermal growth factor, which in monocultures modestly enhanced MCF-7-GFP and markedly increased MCF-10A cell proliferation, greatly inhibited MCF-7-GFP cell proliferation in MCF-10A/MCF-7-GFP cocultures. 17 beta-Estradiol, which stimulated MCF-7-GFP but not MCF-10A cell proliferation in monoculture, inhibited MCF-7-GFP cell proliferation in MCF-10A/MCF-7-GFP cocultures, an effect that was blocked by the antiestrogen, ICI 182,780. On Matrigel, complex MCF-10A/MCF-7-GFP cellular interactions were observed in real time that resulted in the formation of acinus-like structures. These results indicate a role of normal epithelial cells in inhibiting tumor-cell proliferation and demonstrate the utility of this coculture system as a model of early paracrine control of breast cancer. (C) 2006 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.