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	The Von Hippel-Lindau Protein Suppresses Androgen Receptor Activity
	Wang, Jing; Zhang, Wei; Ji, Wei; Liu, Xing; Ouyang, Gang; Xiao, Wuhan
刊名	MOLECULAR ENDOCRINOLOGY
	2014-02-01
卷号	28期号:2页码:239-248
关键词	CELL RENAL-CARCINOMA TUMOR-SUPPRESSOR PROSTATE-CANCER TRANSCRIPTIONAL ACTIVITY GENE-EXPRESSION E3 LIGASE HYPOXIA VHL UBIQUITINATION DEGRADATION
ISSN号	0888-8809
通讯作者	Xiao, WH (reprint author), Chinese Acad Sci, Inst Hydrobiol, Wuhan 430072, Peoples R China.
中文摘要	The androgen receptor (AR) plays a pivotal role in prostate homeostasis and prostate cancer development. To understand the mechanism underlying the regulation of the AR holds a promise for developing novel therapeutic approaches for prostate cancer. Here, we show that the Von Hippel-Lindau gene product, pVHL, physically interacts with AR and inhibits AR transcription activity but does not induce AR turnover. Moreover, pVHL also suppresses androgen-induced cell proliferation, implicating a physiological role of pVHL in androgen-induced signaling pathway. In addition, we provide evidence to show that pVHL actually enhanced AR de-ubiquitination instead of inducing AR ubiquitination, uncovering a noncanonical role of pVHL in the ubiquitin proteasome pathway. Our data reveal a novel function of pVHL in the regulation of AR transcription activity, which may expand the scope of pVHL in tumor suppression and provide mechanistic insight into prostate cancer initiation and progression.
英文摘要	The androgen receptor (AR) plays a pivotal role in prostate homeostasis and prostate cancer development. To understand the mechanism underlying the regulation of the AR holds a promise for developing novel therapeutic approaches for prostate cancer. Here, we show that the Von Hippel-Lindau gene product, pVHL, physically interacts with AR and inhibits AR transcription activity but does not induce AR turnover. Moreover, pVHL also suppresses androgen-induced cell proliferation, implicating a physiological role of pVHL in androgen-induced signaling pathway. In addition, we provide evidence to show that pVHL actually enhanced AR de-ubiquitination instead of inducing AR ubiquitination, uncovering a noncanonical role of pVHL in the ubiquitin proteasome pathway. Our data reveal a novel function of pVHL in the regulation of AR transcription activity, which may expand the scope of pVHL in tumor suppression and provide mechanistic insight into prostate cancer initiation and progression.
WOS标题词	Science & Technology ; Life Sciences & Biomedicine
类目[WOS]	Endocrinology & Metabolism
研究领域[WOS]	Endocrinology & Metabolism
关键词[WOS]	CELL RENAL-CARCINOMA ; TUMOR-SUPPRESSOR ; PROSTATE-CANCER ; TRANSCRIPTIONAL ACTIVITY ; GENE-EXPRESSION ; E3 LIGASE ; HYPOXIA ; VHL ; UBIQUITINATION ; DEGRADATION
收录类别	SCI
资助信息	973 Grant [2010CB126306]; National Natural Science Foundation of China [31071212, 91019008]; Chinese Academy of Sciences Major Scientific and Technological Project [XDA08010208]
语种	英语
WOS记录号	WOS:000331801400008
公开日期	2014-08-13
内容类型	期刊论文
源URL	[http://ir.ihb.ac.cn/handle/342005/20096]
专题	水生生物研究所_水生生物分子与细胞生物学研究中心_期刊论文
作者单位	Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan 430072, Peoples R China
推荐引用方式 GB/T 7714	Wang, Jing,Zhang, Wei,Ji, Wei,et al. The Von Hippel-Lindau Protein Suppresses Androgen Receptor Activity[J]. MOLECULAR ENDOCRINOLOGY,2014,28(2):239-248.
APA	Wang, Jing,Zhang, Wei,Ji, Wei,Liu, Xing,Ouyang, Gang,&Xiao, Wuhan.(2014).The Von Hippel-Lindau Protein Suppresses Androgen Receptor Activity.MOLECULAR ENDOCRINOLOGY,28(2),239-248.
MLA	Wang, Jing,et al."The Von Hippel-Lindau Protein Suppresses Androgen Receptor Activity".MOLECULAR ENDOCRINOLOGY 28.2(2014):239-248.

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