Cicatiello L, Ambrosino C, Coletta B, Scalona M, Sica V, Bresciani F, Weisz A
Istituto di Patologia generale e Oncologia, Prima Facoltà di Medicina e Chirurgia, Università di Napoli, Italy.
J Steroid Biochem Mol Biol. 1992 Mar;41(3-8):523-8. doi: 10.1016/0960-0760(92)90377-u.
Estrogens induce transcriptional activation of c-fos and c-myc proto-oncogenes during mitogenic stimulation of human, chicken, mouse and rat cells in vivo and in vitro. In this paper we show that 17 beta-estradiol injected into adult ovariectomized rats increases c-jun, jun-B and jun-D gene transcription in the uterus. Kinetics and amplitude of response are different for each gene, since c-jun is activated first, within 30 min after injection, followed by jun-D and jun-B, 60 and 90 min after injection, respectively. Maximal activation of jun-B marks a drop in transcription of all the jun genes. Furthermore, transcriptional activation by 17 beta-estradiol of the growth-regulated beta- and gamma-cytoskeletal actin genes is prevented by an inhibitor of protein synthesis, indicating that it is a secondary response to the hormone. These data support the hypothesis that during growth stimulation of target cells the estrogen receptor induces transcription of regulatory genes, triggering in this way a cascade of gene regulation events that results in progression through the cell cycle.
雌激素在体内和体外对人、鸡、小鼠及大鼠细胞进行有丝分裂刺激期间,可诱导c-fos和c-myc原癌基因的转录激活。在本文中,我们表明,给成年去卵巢大鼠注射17β-雌二醇可增加子宫中c-jun、jun-B和jun-D基因的转录。每个基因的反应动力学和幅度各不相同,因为c-jun在注射后30分钟内首先被激活,随后jun-D和jun-B分别在注射后60分钟和90分钟被激活。jun-B的最大激活标志着所有jun基因转录的下降。此外,蛋白质合成抑制剂可阻止17β-雌二醇对生长调节型β-和γ-细胞骨架肌动蛋白基因的转录激活,这表明它是对激素的次级反应。这些数据支持这样一种假说,即在靶细胞生长刺激过程中,雌激素受体诱导调节基因的转录,从而引发一系列基因调控事件,导致细胞周期进程。