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Androgen receptor binding sites identified in mouse testis

生物化学与生物物理学报（英文版） 2013年第9期45卷 795-797页

作者： Shuanggang Hu Guangxin Yao Xiangqi Li Zijiang Chen Yun Sun Department of Reproductive Medicine Ren Ji Hospital School of Medicine Shanghai Jiao Tong University Shanghai 200001 China Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics Shanghai Jiao Tong University Shanghai 200001 China Shanghai Key Laboratory for Molecular Andrology State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China Shanghai Key Laboratory for Molecular Andrology State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China Department of Reproductive Medicine Ren Ji Hospital School of Medicine Shanghai Jiao Tong University Shanghai 200001 China Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics Shanghai Jiao Tong University Shanghai 200001 China

Androgen/androgen receptor (AR) signaling plays decisive roles in testicular spermatogenesis [1].However,the underlying molecular mechanism of androgen and AR regulation (*** genes that are regulated and their functions) remains largely *** analysis combined with androgen treatment or AR knockout animal models has identified androgen-dependent genes in mouse testis [2,3].However,this approach does not distinguish direct and indirect targets of androgen/*** now,only a few AR-binding sites containing androgen responsive elements (AREs) located within the promoter regions of androgen responsive genes in testis have been reported,implying that these genes are direct targets of *** genes include kallikrein 27 (Klk27) [4],reproductive homeobox 5 (Rhox5) [5],epididymal peptidase inhibitor (Eppin) [6],and cytochrome P450,family 17,subfamily a,polypeptide 1 (Cypl7) [7].All of these binding events were demonstrated using in vitro assays including electrophoretic mobility shift assays (EMSA),deoxyribonuclease I footprinting,and luciferase ***,these in vitro measurements cannot be easily extrapolated into in vivo mechanisms,as mammalian genes are commonly organized into broad chromosomal domains,and such domains cannot be readily reconstituted in *** the in vivo assays are greatly required for measuring AR-DNA interactions in testis and understanding the physiological transcriptional *** now,only one AR-binding site associated with tubulin,beta 3 class Ⅲ (Tubb3) gene was identified in mouse testis in vivo using chromatin immunoprecipitation (ChIP) [8].

关键词：基因表达精子发生模型动物受体雄激素/代谢受体雄激素/遗传学微阵列分析睾丸/代谢小鼠动物

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The transcriptional co-activator cAMP response element-binding protein-binding protein is expressed in prostate cancer and enhances androgen- and anti-androgen-induced androgen receptor function

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AMERICAN JOURNAL OF PATHOLOGY 2003年第1期162卷 233-241页

作者： Comuzzi, B Lambrinidis, L Rogatsch, H Godoy-Tundidor, S Knezevic, N Krhen, I Marekovic, Z Bartsch, G Klocker, H Hobisch, A Culig, Z Univ Innsbruck Dept Urol A-6020 Innsbruck Austria Univ Innsbruck Dept Pathol A-6020 Innsbruck Austria Gen Hosp Dept Urol Feldkirch Austria Univ Zagreb Dept Urol Zagreb 41000 Croatia

Progression of human prostate cancer toward therapy resistance occurs in the presence of wild-type or mutated androgen receptors (ARs) that, in some cases, exhibit aberrant activation by various steroid hormones and anti-androgens. The AR associates with a number of co-activators that possess histone acetylase activity and act as bridging molecules to components of the transcription initiation complex. in previous reports, it was shown that the transcriptional co-activator CREB (cAMP response element-binding protein)-binding protein (CBP) enhances AR activity in a ligand-dependent manner. In the present study, we have investigated whether CBP modifies antagonist/agonist balance of the nonsteroidal anti-androgens hydroxyflutamide and bicalutamide. In prostate cancer DU-145 cells, which were transiently transfected with CBP cDNA, hydroxyflutamide enhanced AR activity to a greater extent than bicalutamide in the presence of either wild-type or the mutated AR 730 val-->met. In two sublines of LNCaP cells that contain the mutated AR 877 thr-->ala and overexpressed CBP, Increase in AR activity was observed after treatment with hydroxyflutamide but not with bicalutamide. Anti-androgens did not influence AR expression in cells transfected with CBP cDNA, as judged by Western blot analysis. Endogenous CBP protein was detected by Western blot in nuclear extracts from the three prostate cancer cell lines, LNCaP, PC-3, and DU-145, all derived from therapy-resistant prostate cancer. in addition, CBP was ex pressed in both basal and secretory cells of benign prostate epithelium, high-grade prostate intraepithelial neoplasia, and prostate cancer clinical specimens, as evidenced by immunohistochemical staining. Taken together, our findings demonstrate the selective enhancement of agonistic action of the anti-androgen hydroxyflutamide by the transcriptional co-activator CBP, which is a new, potentially relevant mechanism contributing to the acquisition of therapy resistance in prosta

关键词：雄激素拮抗药/药理学雄激素类/药理学 CREB结合蛋白质癌/代谢癌/病理学淋巴转移核蛋白质类/遗传学前列腺增生/代谢前列腺增生/病理学前列腺肿瘤/代谢前列腺肿瘤/病理学受体雄激素/代谢反式激活因子类/遗传学人类男(雄)性

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Development of an androgen reporter gene assay (AR-LUX) utilizing a human cell line with an endogenously regulated androgen receptor

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ANALYTICAL BIOCHEMISTRY 2001年第1期298卷 93-102页

作者： Blankvoort, BMG de Groene, EM van Meeteren-Kreikamp, AP Witkamp, RF Rodenburg, RJT Aarts, JMMJG TNO Pharma Dept Bioanal NL-3700 AJ Zeist Netherlands Univ Wageningen & Res Ctr Dept Agrotechnol & Food Sci Subdept Toxicol Wageningen Netherlands Unilever Hlth Inst Vlaardingen Netherlands

The aim of the work described in this report is to develop and characterize a cell-based androgen reporter assay. For this purpose, the androgen receptor (AR) expressing human breast cancer cell line T47D was stably transfected with a luciferase gene under transcriptional control of the PB-ARE-2 androgen response element. The application of this cell line in an endogenous Androgen Receptor-mediated LUciferase eXpression assay (ARLUX) was validated. Ain EC50 value of 86 pM was determined for the standard androgen R1881 with a detection limit of 46 pM. Other androgens like dihydrotestosterone, 17 beta -trenbolone, and bolasterone also induced luciferase expression, while anti-androgens suppressed these responses. As expected, AP-mediated responses were also elicited by high concentrations of the steroids progesterone, 17 beta -estradiol, d-aldosterone, and dexamethasone, with observed EC50 values 10 to 350,000 times higher than that for R1881. A unique feature of the AR-LUX assay is that effects on modulation of active endogenous AR-levels are reliably reflected in the luciferase induction response, as exemplified by vitamin D, all-trans-retinoic acid, epigallocatechin gallate, and forskolin. This feature is especially useful when assessing complex mixtures, e.g., environmental samples or natural compound libraries. From these data it is concluded that the AR-LUX assay is a reliable in vitro test system for the detection and quantification of AR-mediated biological effects. The 96-well plate format makes the assay particularly suitable for high-throughput screening. (C) 2001 Academic Press.

关键词：醛固酮/代谢雄激素类/代谢乳腺肿瘤/代谢地塞米松/代谢减量调节雌二醇/代谢基因调节/遗传学基因报告/遗传学基因报告/生理学萤光素酶类/分析萤光素酶类/遗传学萤光素酶类/代谢美曲勃龙/代谢受体雄激素/代谢转染/方法肿瘤细胞培养的/细胞学肿瘤细胞培养的/代谢人类

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Two classes of androgen receptor elements mediate cooperativity through allosteric interactions

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第4期276卷 2943-2952页

作者： Reid, KJ Hendy, SC Saito, J Sorensen, P Nelson, CC Vancouver Gen Hosp Prostate Ctr Vancouver BC Canada

Genes uniquely regulated by the androgen receptor (AR) typically contain multiple androgen response elements (AREs) that in isolation are of low DNA binding affinity and transcriptional activity. However, specific combinations of AREs in their native promoter context result in highly cooperative DNA binding by AR and high levels of transcriptional activation. We demonstrate that the natural androgen-regulated promoters of prostate specific antigen and probasin contain two classes of AREs dictated by their primary nucleotide sequence that function to mediate cooperativity, Class I AR-binding sites display conventional guanine contacts. Class II AR-binding sites have distinctive atypical sequence features and, upon binding to AR, the DNA structure is dramatically altered through allosteric interactions with the receptor. Class II sites stabilize AR binding to adjacent class I sites and result in synergistic transcriptional activity and increased hormone sensitivity. We have determined that the specific nucleotide variation within the AR binding sites dictate differential functions to the receptor, We have identified the role of individual nucleotides within class II sites and predicted consensus sequences for class I and II sites. Our data suggest that this may be a universal mechanism by which AR achieved unique regulation of target genes through complex allosteric interactions dictated by primary binding sequences.

关键词：别构调节雄激素结合蛋白质/遗传学碱基序列结合部位/遗传学分子序列数据诱变定点启动区(遗传学) 前列腺特异抗原/遗传学蛋白质结合受体雄激素/代谢反应元件硫酸酯类/药理学动物大鼠

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Hormone status selects for spontaneous somatic androgen receptor variants that demonstrate specific ligand and cofactor dependent activities in autochthonous prostate cancer

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第14期276卷 11204-11213页

作者： Han, GZ Foster, BA Mistry, S Buchanan, G Harris, JM Tilley, WD Greenberg, NM Baylor Coll Med Dept Mol & Cellular Biol Houston TX 77030 USA Baylor Coll Med Scott Dept Urol Houston TX 77030 USA Flinders Univ S Australia Flinders Canc Ctr Adelaide SA 5042 Australia Flinders Med Ctr Adelaide SA 5042 Australia Univ Queensland Inst Mol Biosci Brisbane Qld 4072 Australia

We have used the autochthonous transgenic adenocarcinoma of mouse prostate (TRAMP) model to investigate the relationship between somatic mutation in the androgen receptor (AR) and the emergence of androgen-independent prostate cancer. Here we report the identification, isolation, and characterization of distinct classes of AR variants from spontaneous prostate tumors in the TRAMP model. Using cDNA cloning, single stranded conformation polymorphism and sequencing strategies, 15 unique somatic mutations in the AR were identified in prostate tumors obtained from eight TRAMP mice between 24 and 29 weeks of age. At least one mutation was isolated from each mouse. All mutations:were single base substitutions, 10 were missense and 5 were silent. Nine mutations in the AR were identified in tumors of four mice that were castrated at 12 weeks of age. Interestingly, the majority of mutations (seven out of nine, 78%) identified in the androgen-independent tumors colocalized in the AR transactivation domain. The remaining mutations colocalized in the AR ligand binding domain. In general, the AR variants demonstrated promoter-, cell-, and cofactor-specific activities in response to various hormones. All AR variants isolated in this study maintained strong sensitivity for androgens, and four AR variants isolated from castrated mice demonstrated increased activities in the absence of ligand. The K638M and F677S variants demonstrated increased activities in response to androgen, and K638M also demonstrated increased response to estradiol, In the presence of AR coactivator ARA70 the E231G variant demonstrated increased activity in response to both androgen and estradiol. However, in the presence of AR coactivator ARA160 the E231G variant was selectively responsive to androgen. Collectively these analyses not only indicate that somatic mutations in the AR gene occur spontaneously in TRAMP tumors but also how changes in the hormonal environment may drive the selection of spontaneous so

关键词：基因表达调控肿瘤配体小鼠转基因模型分子突变前列腺肿瘤/遗传学前列腺肿瘤/代谢受体雄激素/遗传学受体雄激素/代谢信号传导动物男(雄)性小鼠

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Comparative studies of the estrogen receptors β and α and the androgen receptor in normal human prostate glands, dysplasia, and in primary and metastatic carcinoma

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AMERICAN JOURNAL OF PATHOLOGY 2001年第1期159卷 79-92页

作者： Leav, I Lau, KM Adams, JY McNeal, JE Taplin, ME Wang, JF Singh, H Ho, SM Univ Massachusetts Sch Med Dept Surg Div Urol Worcester MA 01655 USA Univ Massachusetts Sch Med Dept Oncol Worcester MA 01655 USA Tufts Univ Sch Med Dept Pathol Boston MA 02111 USA Tufts Univ Sch Vet Med Dept Pathol Boston MA 02111 USA Stanford Univ Med Ctr Dept Urol Stanford CA 94305 USA Biogenex Labs Mt View CA USA

An antibody, GC-17, thoroughly characterized for its specificity for estrogen receptor-beta (ER-beta), was used to immunolocalize the receptor in histologically normal prostate, prostatic intraepithelial neoplasia, primary carcinomas, and in metastases to lymph nodes and bone. Comparisons were made between ER-beta, estrogen receptor-alpha (ER-alpha), and androgen receptor (AR) immunostaining in these tissues. Concurrently, transcript expression of the three steroid hormone receptors was studied by reverse transcriptase-polymerase chain reaction analysis on laser capture-microdissected samples of normal prostatic acini, dysplasias, and carcinomas. In Western blot analyses, GC-17 selectively identified a 63-kd protein expressed In normal and malignant prostatic epithelial cells as well as in normal testicular and prostatic tissues. This protein Likely represents a posttranslationally modified form of the long-form ER-beta, which has a predicted size of 59 kd based on polypeptide length. In normal prostate, ER-beta Immunostaining was predominately localized in the nuclei of basal cells and to a lesser extent stromal cells. ER-alpha staining was only present in stromal cell nuclei. AR immunostaining was variable in basal cells but strongly expressed in nuclei of secretory and stromal cells. Overall, prostatic carcinogenesis was characterized by a loss of ER-beta expression at the protein and transcript levels in high-grade dysplasias, its reappearance in grade 3 cancers, and its diminution/absence in grade 4/5 neoplasms. In contrast, AR was strongly expressed in all grades of dysplasia and carcinoma. Because ER-beta is thought to function as an inhibitor of prostatic growth, androgen action, presumably mediated by functional AR and unopposed by the beta receptor, may have provided a strong stimulus for aberrant cell growth. With the exception of a small subset of dysplasias in the central zone and a few carcinomas, ER-alpha -stained cells were not found in these lesions

关键词：印迹法蛋白质癌/代谢癌/病理学癌/继发性酶联免疫吸附测定雌激素受体α 雌激素受体β 免疫化学免疫组织化学前列腺/代谢前列腺疾病/代谢前列腺肿瘤/代谢前列腺肿瘤/病理学前列腺肿瘤/继发性 RNA 信使/代谢受体雄激素/代谢受体雌激素/遗传学受体雌激素/代谢参考值逆转录聚合酶链反应老年人人类男(雄)性中年人

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Androgen receptor interacts with a novel MYST protein, HBO1

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第45期275卷 35200-35208页

作者： Sharma, M Zarnegar, M Li, XY Lim, B Sun, ZJ Stanford Univ Dept Surg & Genet Sch Med Liem Sioe Liong Mol Biol Lab Stanford CA 94305 USA Beth Israel Deaconess Med Ctr Dept Med Div Hematol Oncol Boston MA 02215 USA

The androgen receptor (AR), a member of the nuclear receptor superfamily, plays a central role in male sexual differentiation and prostate cell proliferation. Results of-treating prostate cancer by androgen ablation indicate that signals mediated through AR are critical for the growth of these tumors. Like other nuclear receptors, AR exerts its transcriptional function by binding to cis-elements upstream of promoters and interacting with. other transcriptional factors (e.g. activators, repressors and modulators). To determine the mechanism of AR-regulated transcription, we used the yeast two-hybrid system to identify AR-associated proteins. One of the proteins we identified is identical to the human origin recognition complex-interacting protein termed HBO1. A ligand-enhanced interaction between AR and HBO1 was further confirmed in vivo and in vitro. Immunofluorescence experiments showed that HBO1 is a nuclear:protein,:and Northern blot analysis revealed that it is ubiquitously expressed, with the highest levels present inhuman testis. HBO1 belongs to the MYST family, which is characterized by a highly conserved C2HC zinc finger and a putative histone acetyltransferase domain. Surprisingly, two yeast members of the MYST family, SAS2: and SAS3, have been shown to function as transcription silencers, despite the presence of the histone acetyltransferase domain. Using a GAL4 DNA-binding domain assay, we mapped a transcriptional repression domain within the N-terminal region of HBO1. Transient transfection experiments revealed that HBO1 specifically repressed AR-mediated transcription in both CV-1 and PC-3 cells. These results indicate that HBO1 is a new AR-interacting protein capable of modulating AR activity. It could play a significant role in regulating AR-dependent genes in normal and prostate cancer cells.

关键词：乙酰基转移酶类/化学乙酰基转移酶类/代谢氨基酸序列印迹法 RNA 印迹法蛋白质细胞系细胞核/代谢 DNA 互补/代谢 DNA结合蛋白质类/化学 DNA结合蛋白质类/代谢电泳聚丙烯酰氨凝胶谷胱甘肽转移酶/代谢直鼻猴亚目组蛋白酰基转移酶配体显微镜检查荧光分子序列数据起点识别复合体质粒/代谢沉淀素试验前列腺肿瘤/代谢蛋白质结合蛋白质结构三级受体雄激素/化学受体雄激素/代谢重组融合蛋白质类/代谢酿酒酵母蛋白质类序列同源性氨基酸睾丸/代谢组织分布转录遗传转染双杂交系统技术锌指动物人类男(雄)性

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Chaperones Hsp70 and Hsp40 suppress aggregate formation and apoptosis in cultured neuronal cells expressing truncated androgen receptor protein with expanded polyglutamine tract

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第12期275卷 8772-8778页

作者： Kobayashi, Y Kume, A Li, M Doyu, M Hata, M Ohtsuka, K Sobue, G Nagoya Univ Sch Med Dept Neurol Showa Ku Nagoya Aichi 4668550 Japan Aichi Canc Ctr Res Inst Expt Radiol Lab Chikusa Ku Nagoya Aichi 4648681 Japan

Spinal and bulbar muscular atrophy (SBMA) is one of a group of human inherited neurodegenerative diseases caused by polyglutamine expansion. We have previously demonstrated that the SBMA gene product, the androgen receptor protein, is toxic and aggregates when truncated. Heat shock proteins function as molecular chaperones, which recognize and renaturate misfolded protein (aggregate). We thus assessed the effect of a variety of chaperones in a cultured neuronal cell model of SBMA. Overexpression of chaperones reduces aggregate formation and suppresses apoptosis in a cultured neuronal cell model of SBMA to differing degrees depending on the chaperones and their combinations. Combination of Hsp70 and Hsp40 was the most effective among the chaperones in reducing aggregate formation and providing cellular protection, reflecting that Hsp70 and Hsp40 act together in chaperoning mutant and disabled proteins. Although Hdj2/Hsdj chaperone has been previously reported to suppress expanded polyglutamine tract-formed aggregate, Hsdj/Hdj2 showed little Effect in our system. These findings indicate that chaperones may be one of the key factors in the developing of CAG repeat disease and suggested that increasing expression level or enhancing the function of chaperones will provide an avenue for the treatment of CAG repeat disease.

关键词：细胞凋亡细胞培养的 HSP40热休克蛋白质类 HSP70热休克蛋白质类/遗传学 HSP70热休克蛋白质类/代谢热休克蛋白质类/遗传学热休克蛋白质类/代谢原位缺口末端标记分子伴侣/遗传学分子伴侣/代谢肌萎缩脊髓性/遗传学神经元/病理学聚谷氨酸/遗传学聚谷氨酸/代谢受体雄激素/遗传学受体雄激素/代谢重组蛋白质类/代谢三核苷酸重复

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Change of specificity mutations in androgen-selective enhancers - Evidence for a role of differential DNA binding by the androgen receptor

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第16期275卷 12298-12305页

作者： Verrijdt, G Schoenmakers, E Haelens, A Peeters, B Verhoeven, G Rombauts, W Claessens, F Katholieke Univ Leuven Fac Med Div Biochem B-3000 Louvain Belgium Katholieke Univ Leuven Fac Med Lab Expt Med & Endocrinol B-3000 Louvain Belgium

The androgen and glucocorticoid receptors recognize identical DNA motifs, leaving unanswered the question of how steroid specificity of transcriptional regulation is established in cells containing both receptors, Here, we protide evidence that subtle differences in low affinity DNA recognition might be a crucial element in the generation of steroid-specific responses. Here we identify simple hormone response elements in the mouse sex-limited protein enhancer and the human secretory component androgen response unit to be essential for the androgen specificity of both enhancers. We describe specific in vitro binding to these motifs by the DNA-binding domain of the androgen but not the glucocorticoid receptor. Both elements can be considered partial direct repeats of the 5'-TGTTCT-3' core binding motif. In addition, we show that specific point mutations in their left half-sites, essentially changing the nature of the repeats, strongly enhance the glucocorticoid sensitivity of the respective enhancers, whereas they have no effect on their androgen responsiveness. Accordingly, these mutations allow specific binding of the glucocorticoid receptor DNA-binding domain to both elements in, vitro. With these experiments, we demonstrate that differential recognition by the androgen receptor of nonconventional steroid response elements is, at least in some cases, an important mechanism in androgen-specific transcriptional regulation.

关键词：结合部位 DNA/代谢增强子元件遗传学/遗传学 HeLa细胞诱变点突变启动区遗传受体雄激素/代谢构效关系转录遗传动物人类小鼠

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Coregulator small nuclear RING finger protein (SNURF) enhances Sp1-and steroid receptor-mediated transcription by different mechanisms

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第1期275卷 571-579页

作者： Poukka, H Aarnisalo, P Santti, H Jänne, OA Palvimo, JJ Univ Helsinki Inst Biomed Dept Physiol FIN-00014 Helsinki Finland Univ Helsinki Dept Clin Chem FIN-00014 Helsinki Finland

The small nuclear RING finger protein SNURF is not only a coactivator in steroid receptor-dependent transcription but also activates transcription from steroid-independent promoters. In this work, we show that SNURF, via the RING finger domain, enhances protein binding to Sp1 elements/GC boxes and interacts and cooperates with Sp1 in transcriptional activation. The activation of androgen receptor (AR) function requires regions other than the RING finger of SNURF, and SNURF does not influence binding of AR to cognate DNA elements. The zinc finger region (ZFR) together with the hinge region of AR are sufficient for contacting SNURF. The nuclear localization signal in the boundary between ZFR and the hinge region participates in the association of AR with SNURF, and a receptor mutant lacking the C-terminal part of the bipartite nuclear localization signal shows attenuated response to coexpressed SNURF. Some AR ZFR point mutations observed in patients with partial androgen insensitivity syndrome or male breast cancer impair the interaction of AR with SNURF and also render AR refractory to the transcription-activating effect of SNURF. Collectively, SNURF modulates the transcriptional activities of androgen receptor and Sp1 via different domains, and it may act as a functional link between steroid- and Sp1-regulated transcription.

关键词：氨基酸序列雄激素迟钝综合征/遗传学乳腺肿瘤男性/遗传学 DNA结合蛋白质类/代谢基因表达调控分子序列数据核定位信号核蛋白质类/遗传学核蛋白质类/代谢点突变启动区遗传蛋白质结合受体雄激素/代谢重组蛋白质类/代谢 Sp1转录因子/代谢转录因子/遗传学转录因子/代谢转录遗传锌指/遗传学人类男(雄)性

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