Pourreau-Schneider N, Delori P, Boutière B, Arnoux D, George F, Sampol J, Martin P M
CNRS URA 201, Faculté de Médecine Nord, Marseille, France.
J Natl Cancer Inst. 1989 Feb 15;81(4):259-66. doi: 10.1093/jnci/81.4.259.
We have analyzed the plasminogen activator (PA) systems of two metastatic breast adenocarcinoma cell lines, MCF-7 and MDA-MB-231, as a function of 17 beta-estradiol stimulation when the cells were cultured on purified components of extracellular matrix. Laminin enhanced PA levels in both cell lines, but this enhancement seemed to occur via different mechanisms, including dissociation of inhibitor complexes. The major effect was the marked increase in cell-associated urokinase-type PA (u-PA); the increase was independent of estrogen in hormone-insensitive MDA-MB-231 cells grown on laminin-coated surfaces. In estrogen-sensitive MCF-7 cells, 17 beta-estradiol stimulated u-PA secretion in a similar fashion on plastic, laminin, fibronectin, or collagen but acted in synergy with laminin in the production and release of tissue-type PA.
我们分析了两种转移性乳腺腺癌细胞系MCF-7和MDA-MB-231的纤溶酶原激活剂(PA)系统,该系统是细胞在细胞外基质的纯化成分上培养时17β-雌二醇刺激作用的函数。层粘连蛋白可提高两种细胞系中的PA水平,但这种提高似乎是通过不同机制发生的,包括抑制剂复合物的解离。主要作用是细胞相关尿激酶型PA(u-PA)显著增加;在层粘连蛋白包被表面生长的激素不敏感型MDA-MB-231细胞中,这种增加与雌激素无关。在雌激素敏感型MCF-7细胞中,17β-雌二醇在塑料、层粘连蛋白、纤连蛋白或胶原蛋白上以类似方式刺激u-PA分泌,但在组织型PA的产生和释放方面与层粘连蛋白协同作用。