Shafie S, Brooks S C
Cancer Res. 1977 Mar;37(3):792-9.
The intracellular specific 17beta-estradiol binding in the human breast cancer cell line, MCF-7, was shown to be modified by prolactin. Both ovine and human prolactin doubled the estradiol receptor (E2R) level, but the latter was at least 10 times more stimulatory on a concentration basis. Most of the E2R complex (approximately 80%) was transported to the nucleus, and the prolactin stimulation was reflected in an elevated nuclear uptake of the tritiated 17beta-estradiol. Neither ovine nor human prolactin altered the growth rate of the cells when E2R stimulation was maximal. Insulin (10 mug/ml) stimulated tritiated thymidine incorporation and total DNA content but had no apparent effect on E2R concentration. At 10(-4) M, N6,O2'-dibutyrylcyclicadenosine 3':5'-monophosphate increased insulin stimulation of tritiated thymidine incorporation and brought about a prolactin stimulation of apparent DNA synthesis. Theophylline (10(-3) M) blocked both of these effects of N6,O2'-dibutyrylcyclicadenosine 3':5'-monophosphate. The possible mechanism implicating prolactin as an effector of differentiation and growth of MCF-7 cells is discussed.
在人乳腺癌细胞系MCF - 7中，细胞内特异性17β - 雌二醇结合被证明会受到催乳素的影响。绵羊催乳素和人催乳素均可使雌二醇受体（E2R）水平加倍，但就浓度而言，后者的刺激作用至少强10倍。大部分E2R复合物（约80%）被转运至细胞核，催乳素的刺激作用表现为氚标记的17β - 雌二醇核摄取增加。当E2R刺激达到最大时，绵羊催乳素和人催乳素均未改变细胞的生长速率。胰岛素（10微克/毫升）刺激了氚标记胸腺嘧啶核苷的掺入和总DNA含量，但对E2R浓度无明显影响。在10⁻⁴ M时，N⁶,O²'-二丁酰环腺苷3':5'-单磷酸增强了胰岛素对氚标记胸腺嘧啶核苷掺入的刺激作用，并引发了催乳素对明显DNA合成的刺激作用。茶碱（10⁻³ M）阻断了N⁶,O²'-二丁酰环腺苷3':5'-单磷酸的这两种作用。文中讨论了催乳素作为MCF - 7细胞分化和生长效应器的可能机制。
