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来自大鼠催乳素基因5'侧翼区域的雌激素反应元件在MCF-7细胞中起作用,但在HeLa细胞中不起作用。

An estrogen-responsive element from the 5'-flanking region of the rat prolactin gene functions in MCF-7 but not in HeLa cells.

作者信息

Somasekhar M B, Gorski J

机构信息

Department of Biochemistry, College of Agriculture and Life Sciences, University of Wisconsin-Madison 53706.

出版信息

Gene. 1988 Sep 15;69(1):23-8. doi: 10.1016/0378-1119(88)90374-5.

DOI:10.1016/0378-1119(88)90374-5
PMID:3224823
Abstract

We have used MCF-7, the human breast cancer cell line, which is estrogen receptor-positive, and the HeLa cell line, which is estrogen receptor-negative, to study the mechanisms by which estrogen induces prolactin gene transcription. A series of plasmids were constructed which direct the expression of the easily assayed bacterial enzyme chloramphenicol acetyltransferase. We have used these recombinants to show that the estrogen-responsive DNA element (ERE) required for the estrogenic regulation of the rat prolactin gene is functional in MCF-7 cells but not in HeLa cells. Specifically, in MCF-7 cells this element enhances the level of gene activity after estrogen treatment both from its own promoter and from a heterologous (simian virus 40) promoter. Results of these studies also show that in HeLa cells the ERE can mediate estrogenic regulation if cotransfected with a plasmid that can synthesize estrogen receptor.

摘要

我们使用了雌激素受体阳性的人乳腺癌细胞系MCF - 7和雌激素受体阴性的HeLa细胞系,来研究雌激素诱导催乳素基因转录的机制。构建了一系列指导易于检测的细菌酶氯霉素乙酰转移酶表达的质粒。我们利用这些重组体表明,大鼠催乳素基因雌激素调节所需的雌激素反应性DNA元件(ERE)在MCF - 7细胞中具有功能,但在HeLa细胞中则没有。具体而言,在MCF - 7细胞中,该元件在雌激素处理后,既能增强其自身启动子的基因活性水平,也能增强异源(猿猴病毒40)启动子的基因活性水平。这些研究结果还表明,在HeLa细胞中,如果与能合成雌激素受体的质粒共转染,ERE可以介导雌激素调节。

相似文献

1
An estrogen-responsive element from the 5'-flanking region of the rat prolactin gene functions in MCF-7 but not in HeLa cells.来自大鼠催乳素基因5'侧翼区域的雌激素反应元件在MCF-7细胞中起作用,但在HeLa细胞中不起作用。
Gene. 1988 Sep 15;69(1):23-8. doi: 10.1016/0378-1119(88)90374-5.
2
Regulation of pS2 gene expression by affinity labeling and reversibly binding estrogens and antiestrogens: comparison of effects on the native gene and on pS2-chloramphenicol acetyltransferase fusion genes transfected into MCF-7 human breast cancer cells.通过亲和标记以及可逆结合的雌激素和抗雌激素对pS2基因表达的调控:对天然基因以及转染到MCF-7人乳腺癌细胞中的pS2-氯霉素乙酰转移酶融合基因的作用比较
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Hormonal regulation of the bovine prolactin promoter in rat pituitary tumor cells.
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Identification of an estrogen-responsive element from the 5'-flanking region of the rat prolactin gene.从大鼠催乳素基因5'侧翼区鉴定雌激素反应元件。
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Two elements of the rat prolactin 5' flanking region are required for its regulation by estrogen and glucocorticoids.大鼠催乳素5'侧翼区的两个元件是其受雌激素和糖皮质激素调控所必需的。
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Estrogen stimulates transcription from the human prolactin distal promoter through AP1 and estrogen responsive elements in T47D human breast cancer cells.雌激素通过激活蛋白1(AP1)和雌激素反应元件,刺激T47D人乳腺癌细胞中人类催乳素远端启动子的转录。
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Identification of a novel transferable cis element in the promoter of an estrogen-responsive gene that modulates sensitivity to hormone and antihormone.在一个雌激素反应基因的启动子中鉴定出一种新型可转移顺式元件,该元件可调节对激素和抗激素的敏感性。
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Regulation by estrogen through the 5'-flanking region of the mouse calbindin-D28k gene.雌激素通过小鼠钙结合蛋白-D28k基因的5'-侧翼区域进行调控。
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Comparison of the estrogen responsiveness of the rat and bovine oxytocin gene promoters.大鼠和牛催产素基因启动子雌激素反应性的比较。
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Inhibition of estrogen-induced activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the MCF-7 human breast cancer and other cell lines transfected with vitellogenin A2 gene promoter constructs.2,3,7,8-四氯二苯并对二恶英(TCDD)对雌激素诱导活性的抑制作用,该作用发生在转染了卵黄蛋白原A2基因启动子构建体的MCF-7人乳腺癌细胞系及其他细胞系中。
Arch Biochem Biophys. 1997 Feb 1;338(1):67-72. doi: 10.1006/abbi.1996.9806.

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The orphan nuclear receptor estrogen-related receptor alpha is a transcriptional regulator of the human medium-chain acyl coenzyme A dehydrogenase gene.孤儿核受体雌激素相关受体α是人类中链酰基辅酶A脱氢酶基因的转录调节因子。
Mol Cell Biol. 1997 Sep;17(9):5400-9. doi: 10.1128/MCB.17.9.5400.
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Inhibition of estrogen-responsive gene activation by the retinoid X receptor beta: evidence for multiple inhibitory pathways.维甲酸X受体β对雌激素反应性基因激活的抑制作用:多条抑制途径的证据。
Mol Cell Biol. 1993 Apr;13(4):2258-68. doi: 10.1128/mcb.13.4.2258-2268.1993.