Chasserot-Golaz S, Beck G, Venetianer A
Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
Mol Cell Endocrinol. 1991 Dec;82(2-3):151-8. doi: 10.1016/0303-7207(91)90026-o.
The synthetic steroid RU486 (17 beta-hydroxy-11 beta-(4-dimethylaminophenyl)-17 alpha-(1-propynyl)-estra-4,9-dien-3-one), which has been shown to display antiprogestin and antiglucocorticoid properties in different systems, exerts antiglucocorticoid effects and inhibits the cell growth in a concentration-dependent manner on Reuber rat hepatoma cell variants. This effect can be observed on glucocorticoid-sensitive cells, containing glucocorticoid receptors, and on glucocorticoid-resistant cells displaying a very low level of dexamethasone binding. Metabolization of RU486 occurs in different glucocorticoid-resistant hepatoma variants; these cells are less sensitive to the growth inhibitory effect of the antihormone than the steroid-sensitive cells which do not metabolize RU486. Thus, metabolization of RU486 must also be taken into account for the efficacy of this antagonist on cell growth.
合成类固醇RU486（17β-羟基-11β-（4-二甲基氨基苯基）-17α-（1-丙炔基）-雌甾-4,9-二烯-3-酮）已被证明在不同系统中具有抗孕激素和抗糖皮质激素特性，它对鲁伯大鼠肝癌细胞变体具有抗糖皮质激素作用，并以浓度依赖的方式抑制细胞生长。这种作用在含有糖皮质激素受体的糖皮质激素敏感细胞以及显示地塞米松结合水平极低的糖皮质激素抗性细胞中均可观察到。RU486在不同的糖皮质激素抗性肝癌变体中发生代谢；与不代谢RU486的类固醇敏感细胞相比，这些细胞对抗激素的生长抑制作用不太敏感。因此，在考虑这种拮抗剂对细胞生长的功效时，也必须考虑RU486的代谢情况。
