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网格蛋白基因表达在前列腺中受雄激素调控。

Clathrin gene expression is androgen regulated in the prostate.

作者信息

Prescott J L, Tindall D J

机构信息

Department of Biochemistry and Molecular Biology, Mayo Foundation, Rochester, Minnesota 55905, USA.

出版信息

Endocrinology. 1998 Apr;139(4):2111-9. doi: 10.1210/endo.139.4.5926.

DOI:10.1210/endo.139.4.5926
PMID:9529000
Abstract

Androgens are required for the development and function of the prostate. In a normal human prostate, androgens control the synthesis of proteins such as prostate-specific antigen and human glandular kallikrein. The prostate secretes these proteins as well as a number of other compounds to form the prostatic fluid. Using differential display PCR to detect novel androgen-regulated genes, clathrin heavy chain expression was identified as potentially being up-regulated by androgens in the prostate cancer cell line LNCaP. We report here that the clathrin heavy chain and light chain genes are regulated by androgens. Clathrin heavy chain messenger RNA was up-regulated by androgens in a concentration- and time-specific manner in the LNCaP cell line. Translation of clathrin heavy chain messenger RNA was stimulated by androgens. Steady state levels of clathrin light chains a and b were up-regulated in the presence of androgen in LNCaP cells. Clathrin gene expression was examined in normal rat prostates, and similar results were found. Clathrin heavy chain protein levels in the rat prostate are also affected by the androgen status of the animal. We hypothesize that clathrin may be involved in the exocytosis of androgen-regulated secretory proteins such as prostate-specific antigen and human glandular kallikrein.

摘要

雄激素对于前列腺的发育和功能至关重要。在正常人类前列腺中,雄激素控制前列腺特异性抗原和人腺体激肽释放酶等蛋白质的合成。前列腺分泌这些蛋白质以及许多其他化合物以形成前列腺液。利用差异显示PCR检测新的雄激素调节基因,发现网格蛋白重链表达在前列腺癌细胞系LNCaP中可能被雄激素上调。我们在此报告,网格蛋白重链和轻链基因受雄激素调节。在LNCaP细胞系中,雄激素以浓度和时间特异性方式上调网格蛋白重链信使RNA。雄激素刺激网格蛋白重链信使RNA的翻译。在LNCaP细胞中,雄激素存在时网格蛋白轻链a和b的稳态水平上调。在正常大鼠前列腺中检测了网格蛋白基因表达,发现了类似结果。大鼠前列腺中网格蛋白重链蛋白水平也受动物雄激素状态的影响。我们推测,网格蛋白可能参与雄激素调节的分泌蛋白如前列腺特异性抗原和人腺体激肽释放酶的胞吐作用。

相似文献

1
Clathrin gene expression is androgen regulated in the prostate.网格蛋白基因表达在前列腺中受雄激素调控。
Endocrinology. 1998 Apr;139(4):2111-9. doi: 10.1210/endo.139.4.5926.
2
A novel androgen-regulated gene, PMEPA1, located on chromosome 20q13 exhibits high level expression in prostate.一个位于20号染色体q13区域的新型雄激素调节基因PMEPA1在前列腺中呈现高水平表达。
Genomics. 2000 Jun 15;66(3):257-63. doi: 10.1006/geno.2000.6214.
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Androgen regulation of the messenger RNA encoding diazepam-binding inhibitor/acyl-CoA-binding protein in the human prostatic adenocarcinoma cell line LNCaP.雄激素对人前列腺癌细胞系LNCaP中编码地西泮结合抑制剂/酰基辅酶A结合蛋白的信使核糖核酸的调控。
Mol Cell Endocrinol. 1994 Sep;104(2):153-62. doi: 10.1016/0303-7207(94)90118-x.
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Androgens stimulate fatty acid synthase in the human prostate cancer cell line LNCaP.雄激素可刺激人前列腺癌细胞系LNCaP中的脂肪酸合酶。
Cancer Res. 1997 Mar 15;57(6):1086-90.
5
Transcriptional regulation of prostate kallikrein-like genes by androgen.
Mol Endocrinol. 1992 May;6(5):753-62. doi: 10.1210/mend.6.5.1376410.
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Peroxisome proliferator-activated receptor alpha is an androgen-responsive gene in human prostate and is highly expressed in prostatic adenocarcinoma.过氧化物酶体增殖物激活受体α是人类前列腺中的一种雄激素反应性基因,在前列腺腺癌中高度表达。
Clin Cancer Res. 2000 Aug;6(8):3241-8.
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Identification and characterization of PLZF as a prostatic androgen-responsive gene.PLZF作为前列腺雄激素反应基因的鉴定与特征分析。
Prostate. 2004 Jun 1;59(4):426-35. doi: 10.1002/pros.20000.
8
Androgens up-regulate the human prostate-specific antigen messenger ribonucleic acid (mRNA), but down-regulate the prostatic acid phosphatase mRNA in the LNCaP cell line.雄激素可上调人前列腺特异性抗原信使核糖核酸(mRNA),但下调LNCaP细胞系中的前列腺酸性磷酸酶mRNA。
Endocrinology. 1992 Feb;130(2):766-72. doi: 10.1210/endo.130.2.1370795.
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Growth factor regulation of gene expression in the human prostatic carcinoma cell line LNCaP.人前列腺癌细胞系LNCaP中基因表达的生长因子调控
Cancer Res. 1993 Mar 1;53(5):1051-8.
10
Liprin-alpha2 gene, protein tyrosine phosphatase LAR interacting protein related gene, is downregulated by androgens in the human prostate cancer cell line LNCaP.脂磷素α2基因,即蛋白酪氨酸磷酸酶LAR相互作用蛋白相关基因,在人前列腺癌细胞系LNCaP中受雄激素下调。
Int J Mol Med. 2002 Aug;10(2):173-6.

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