中文摘要：

目的探讨雌二醇／孕激素联合方案对人乳腺癌细胞MCF-7和MCF-7／PGRMCl（wT-12）增殖的影响。方法MCF-7细胞，用表达PGRMCl的质粒稳定转染到MCF-7细胞，使其成为MCF-7／wT-12乳腺癌细胞。雌二醇浓度（10^10M，10^-12M，10^14M）与孕酮、合成孕激素安宫黄体酮、炔诺酮序贯联合加入上述两种人乳腺癌细胞进行培养6天，M1Tr法分别测定MCF-7、MCF-7／WT-12肿瘤细胞的生长增殖情况。结果单纯雌二醇在高浓度10^-10M下，明显刺激细胞生长，这种生长不受加入各种孕激素的影响。单纯雌二醇在低浓度下10^-12。M、10^-14。M下对MCF-7及MCF-7／wT-12细胞刺激增殖作用轻微或没有明显刺激细胞增殖的作用，然而，加用炔诺酮则可激发细胞明显的增殖反应，而增加安宫黄体酮和孕酮则显示中性作用，无激发反应。MCF-7／WT-12细胞的增殖反应更明显。结论雌二醇在表达孕激素受体膜组分1（progesteronereceptormembranecomponent1，PGRMCI）的MCF-7细胞中能明显诱发细胞增殖的增加，且表现为剂量依赖性。在低的雌二醇浓度下，某些孕激素可能启动了一种强增殖信号。关于HRT低剂量雌二醇致乳腺癌风险增加的可能性，可能与用某些特殊的孕激素有关。

英文摘要：

Objective To investigate the effect of estradiol/progestogen combinations on MCF -7 and MCF -7 breast cancer cells overexpressing progesterone receptor membrane component 1 （ PGRMC1 ）. Methods MCF - 7 cells were stably transfected with PGRMC1 expression plasmid （MCF -7/PGRMC1 -3HA）. Estradiol （10^-10M, 10^-12M, 10^-14 M） was sequentially combined with progesterone （P10^-7 M） or the synthetic progestins medroxyprogesterone acetate （MPA 10^-7M）, and norethisterone （NET 10^-7M）. Cell proliferation was investigated in MCF - 7 and MCF - 7/WT - 12 ceils. Results In sequential combination, E2 alone elicited a significant proliferative increase at 10^-10 M. This increase was not significantly influenced by the addition of the various progestogens. However, E2 alone at the lower concentrations of 10^-12M and 10^-14M showed no significant effect or slight increased effects on the proliferation of MCF - 7 and MCF - 7/WT - 12 cells, whereby addition of NET triggered a significant proliferative response, in contrast P and MPA were neutral in this action, i.e. elicited no effect, this effect of proliferation is much more significant on MCF -7/WT - 12 cells in contrast on MCF -7 cells. Conclusion Estradiol dose -dependently elicited a strong proliferative increase in MCF -7 cells overexpressing progesterone receptor membrane component 1 （PGRMC1）. At lower concentrations of estradiol, certain progestogens were able to trigger a strong proliferative signal. Concerning the possible increase of breast cancer risk during hormone therapy caused by low estradiol dosages, the use of specific progestogens might be of crucial relevance.