• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

雄激素受体信号拮抗剂 DL3 和抗雄激素比卡鲁胺优先诱导雄激素反应性人前列腺癌细胞 G1 期阻滞。

Preferential induction of G1 arrest in androgen-responsive human prostate cancer cells by androgen receptor signaling antagonists DL3 and antiandrogen bicalutamide.

机构信息

Department of Internal Medicine, The University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.

出版信息

Cancer Lett. 2010 Dec 8;298(2):250-7. doi: 10.1016/j.canlet.2010.07.012. Epub 2010 Aug 2.

DOI:10.1016/j.canlet.2010.07.012
PMID:20675041
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2956783/
Abstract

The purpose of this study was to further characterize cell growth-inhibitory effects of a recently identified androgen receptor (AR) signaling inhibitor 6-amino-2-[2-(4-tert-butyl-pnenoxy)-ethylsulfanyl]-1H-pyrimidin-4-one (DL3)(5) and antiandrogen bicalutamide (Bic). DL3 was more potent than Bic in induction of G1 arrest and reduction of G1-related cell cycle protein expression in AR-positive LNCaP cells. DL3, but not Bic, moderately inhibited growth of AR-negative PC-3 cells independent of G1 arrest. The data indicated that DL3 inhibit cell growth in both AR-dependent and -independent manners and is potentially a potent therapeutic agent for the management of advanced human prostate cancer.

摘要

本研究的目的是进一步描述最近发现的雄激素受体（AR）信号抑制剂 6-氨基-2-[2-（4-叔丁基苯氧基）-乙基硫代]-1H-嘧啶-4-酮（DL3）（5）和抗雄激素比卡鲁胺（Bic）的细胞生长抑制作用。在诱导 AR 阳性 LNCaP 细胞 G1 期阻滞和降低 G1 期相关细胞周期蛋白表达方面，DL3 比 Bic 更有效。DL3 而非 Bic 可独立于 G1 期阻滞，适度抑制 AR 阴性 PC-3 细胞的生长。数据表明，DL3 以 AR 依赖和非依赖的方式抑制细胞生长，是治疗晚期人前列腺癌的潜在有效药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81fe/2956783/23ab62602e99/nihms226102f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81fe/2956783/50d0f68e0abc/nihms226102f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81fe/2956783/e1df27e178db/nihms226102f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81fe/2956783/60df52d735ae/nihms226102f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81fe/2956783/23ab62602e99/nihms226102f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81fe/2956783/50d0f68e0abc/nihms226102f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81fe/2956783/e1df27e178db/nihms226102f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81fe/2956783/60df52d735ae/nihms226102f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81fe/2956783/23ab62602e99/nihms226102f4.jpg

相似文献

1
Preferential induction of G1 arrest in androgen-responsive human prostate cancer cells by androgen receptor signaling antagonists DL3 and antiandrogen bicalutamide.雄激素受体信号拮抗剂 DL3 和抗雄激素比卡鲁胺优先诱导雄激素反应性人前列腺癌细胞 G1 期阻滞。
Cancer Lett. 2010 Dec 8;298(2):250-7. doi: 10.1016/j.canlet.2010.07.012. Epub 2010 Aug 2.
2
A novel synthetic compound that interrupts androgen receptor signaling in human prostate cancer cells.一种新型合成化合物，可阻断人前列腺癌细胞中的雄激素受体信号传导。
Mol Cancer Ther. 2007 Jul;6(7):2057-64. doi: 10.1158/1535-7163.MCT-06-0735.
3
Galbanic acid decreases androgen receptor abundance and signaling and induces G1 arrest in prostate cancer cells.獐牙菜苦酸降低雄激素受体丰度和信号转导，并诱导前列腺癌细胞 G1 期停滞。
Int J Cancer. 2012 Jan 1;130(1):200-12. doi: 10.1002/ijc.25993. Epub 2011 May 9.
4
Antagonistic interaction between bicalutamide (Casodex) and radiation in androgen-positive prostate cancer LNCaP cells.比卡鲁胺（康士得）与放射疗法在雄激素阳性前列腺癌细胞系 LNCaP 中的拮抗作用。
Prostate. 2010 Mar 1;70(4):401-11. doi: 10.1002/pros.21074.
5
Chronic azacitidine treatment results in differentiating effects, sensitizes against bicalutamide in androgen-independent prostate cancer cells.长期使用阿扎胞苷治疗会产生分化作用，使去势抵抗性前列腺癌细胞对比卡鲁胺敏感。
Prostate. 2008 May 15;68(7):793-801. doi: 10.1002/pros.20748.
6
Metformin represses androgen-dependent and androgen-independent prostate cancers by targeting androgen receptor.二甲双胍通过靶向雄激素受体抑制雄激素依赖性和非雄激素依赖性前列腺癌。
Prostate. 2015 Aug 1;75(11):1187-96. doi: 10.1002/pros.23000. Epub 2015 Apr 20.
7
Preclinical pharmacology of FL442, a novel nonsteroidal androgen receptor modulator.新型非甾体雄激素受体调节剂FL442的临床前药理学
Mol Cell Endocrinol. 2014 Apr 25;387(1-2):8-18. doi: 10.1016/j.mce.2014.02.008. Epub 2014 Feb 22.
8
A competitive inhibitor that reduces recruitment of androgen receptor to androgen-responsive genes.一种竞争性抑制剂，可减少雄激素受体向雄激素反应基因的募集。
J Biol Chem. 2012 Jul 6;287(28):23368-80. doi: 10.1074/jbc.M112.344671. Epub 2012 May 15.
9
Effects of treatment with androgen receptor ligands on microRNA expression of prostate cancer cells.雄激素受体配体治疗对前列腺癌细胞微小RNA表达的影响。
Toxicology. 2015 Jul 3;333:45-52. doi: 10.1016/j.tox.2015.04.002. Epub 2015 Apr 3.
10
Induction of bicalutamide sensitivity in prostate cancer cells by an epigenetic Puralpha-mediated decrease in androgen receptor levels.表观遗传 Puralpha 介导的雄激素受体水平降低诱导前列腺癌细胞对比卡鲁胺的敏感性。
Prostate. 2010 Feb 1;70(2):179-89. doi: 10.1002/pros.21051.

引用本文的文献

1
NEK1 Phosphorylation of YAP Promotes Its Stabilization and Transcriptional Output.NEK1对YAP的磷酸化促进其稳定性和转录输出。
Cancers (Basel). 2020 Dec 7;12(12):3666. doi: 10.3390/cancers12123666.
2
Expression of FGD4 positively correlates with the aggressive phenotype of prostate cancer.FGD4 的表达与前列腺癌的侵袭表型呈正相关。
BMC Cancer. 2018 Dec 17;18(1):1257. doi: 10.1186/s12885-018-5096-9.

本文引用的文献

1
Non-competitive androgen receptor inhibition in vitro and in vivo.体外和体内的非竞争性雄激素受体抑制
Proc Natl Acad Sci U S A. 2009 Apr 28;106(17):7233-8. doi: 10.1073/pnas.0807282106. Epub 2009 Apr 10.
2
Development of a second-generation antiandrogen for treatment of advanced prostate cancer.开发用于治疗晚期前列腺癌的第二代抗雄激素药物。
Science. 2009 May 8;324(5928):787-90. doi: 10.1126/science.1168175. Epub 2009 Apr 9.
3
AR, the cell cycle, and prostate cancer.雄激素受体、细胞周期与前列腺癌
Nucl Recept Signal. 2008 Feb 1;6:e001. doi: 10.1621/nrs.06001.
4
A novel synthetic compound that interrupts androgen receptor signaling in human prostate cancer cells.一种新型合成化合物，可阻断人前列腺癌细胞中的雄激素受体信号传导。
Mol Cancer Ther. 2007 Jul;6(7):2057-64. doi: 10.1158/1535-7163.MCT-06-0735.
5
Therapeutic potential of CDK inhibitor NU2058 in androgen-independent prostate cancer.CDK抑制剂NU2058在雄激素非依赖性前列腺癌中的治疗潜力
Oncogene. 2007 Dec 6;26(55):7611-9. doi: 10.1038/sj.onc.1210586. Epub 2007 Jun 18.
6
The complex role of AR signaling after cytotoxic insult: implications for cell-cycle-based chemotherapeutics.细胞毒性损伤后雄激素受体信号传导的复杂作用：对基于细胞周期的化疗的影响。
Cell Cycle. 2007 Jun 1;6(11):1307-13. doi: 10.4161/cc.6.11.4353. Epub 2007 Jun 26.
7
Down-regulation of androgen receptor by 3,3'-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells.3,3'-二吲哚甲烷对雄激素受体的下调作用有助于抑制激素敏感的LNCaP和不敏感的C4-2B前列腺癌细胞的增殖并诱导其凋亡。
Cancer Res. 2006 Oct 15;66(20):10064-72. doi: 10.1158/0008-5472.CAN-06-2011.
8
Inhibition of androgen receptor signaling by selenite and methylseleninic acid in prostate cancer cells: two distinct mechanisms of action.亚硒酸盐和甲基亚硒酸对前列腺癌细胞雄激素受体信号传导的抑制作用：两种不同的作用机制。
Mol Cancer Ther. 2006 Aug;5(8):2078-85. doi: 10.1158/1535-7163.MCT-06-0056.
9
Androgens induce prostate cancer cell proliferation through mammalian target of rapamycin activation and post-transcriptional increases in cyclin D proteins.雄激素通过雷帕霉素哺乳动物靶点激活和细胞周期蛋白D蛋白的转录后增加来诱导前列腺癌细胞增殖。
Cancer Res. 2006 Aug 1;66(15):7783-92. doi: 10.1158/0008-5472.CAN-05-4472.
10
Vav3 oncogene is overexpressed and regulates cell growth and androgen receptor activity in human prostate cancer.Vav3癌基因在人类前列腺癌中过度表达，并调节细胞生长和雄激素受体活性。
Mol Endocrinol. 2006 Oct;20(10):2315-25. doi: 10.1210/me.2006-0048. Epub 2006 Jun 8.