Davidson N E, Bronzert D A, Chambon P, Gelmann E P, Lippman M E
Cancer Res. 1986 Apr;46(4 Pt 2):1904-8.
Two variants of the human estrogen-responsive breast cancer cell line MCF-7, were utilized to study the expression of an estrogen-induced gene, pS2, and an estrogen-induced Mr 52,000 protein. One variant cell line, I13, is growth inhibited after chronic exposure to estrogen. Both the pS2 gene product and the Mr 52,000 protein were produced at maximal levels at a time when I13 growth was inhibited by estrogen. The variant cell line, LY2, selected for its resistance to the growth-inhibitory effects of the antiestrogen, LY117018, grew normally in the presence of this drug, although both pS2 expression and Mr 52,000 protein production were inhibited. These results confirm that the pS2 gene and Mr 52,000 protein are estrogen-regulated elements, but the lack of correlation between their activities and variant cell growth suggests that they are not major autocrine growth-stimulatory agents.
利用人雌激素反应性乳腺癌细胞系MCF-7的两个变体，研究雌激素诱导基因pS2和雌激素诱导的52000分子量蛋白的表达。一个变体细胞系I13，在长期暴露于雌激素后生长受到抑制。当I13的生长被雌激素抑制时，pS2基因产物和52000分子量蛋白均以最大水平产生。变体细胞系LY2，因其对抗雌激素LY117018的生长抑制作用具有抗性而被挑选出来，在这种药物存在的情况下正常生长，尽管pS2表达和52000分子量蛋白的产生均受到抑制。这些结果证实pS2基因和52000分子量蛋白是雌激素调节元件，但它们的活性与变体细胞生长之间缺乏相关性，这表明它们不是主要的自分泌生长刺激剂。
