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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; Xiao, WH (reprint author), Chinese Acad Sci, Inst Hydrobiol, Wuhan 430072, Peoples R China.
2014-02-01
Source PublicationMOLECULAR ENDOCRINOLOGY
ISSN0888-8809
Volume28Issue:2Pages:239-248
AbstractThe 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.; 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.
SubtypeArticle
KeywordCell Renal-carcinoma Tumor-suppressor Prostate-cancer Transcriptional Activity Gene-expression E3 Ligase Hypoxia Vhl Ubiquitination Degradation
Department[Wang, Jing; Zhang, Wei; Ji, Wei; Liu, Xing; Ouyang, Gang; Xiao, Wuhan] Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan 430072, Peoples R China
DOI10.1210/me.2013-1258
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Funding Organization973 Grant [2010CB126306]; National Natural Science Foundation of China [31071212, 91019008]; Chinese Academy of Sciences Major Scientific and Technological Project [XDA08010208] ; 973 Grant [2010CB126306]; National Natural Science Foundation of China [31071212, 91019008]; Chinese Academy of Sciences Major Scientific and Technological Project [XDA08010208] ; 973 Grant [2010CB126306]; National Natural Science Foundation of China [31071212, 91019008]; Chinese Academy of Sciences Major Scientific and Technological Project [XDA08010208] ; 973 Grant [2010CB126306]; National Natural Science Foundation of China [31071212, 91019008]; Chinese Academy of Sciences Major Scientific and Technological Project [XDA08010208]
Indexed BySCI
Language英语
WOS Research AreaEndocrinology & Metabolism
WOS SubjectEndocrinology & Metabolism
WOS IDWOS:000331801400008
WOS KeywordCELL RENAL-CARCINOMA ; TUMOR-SUPPRESSOR ; PROSTATE-CANCER ; TRANSCRIPTIONAL ACTIVITY ; GENE-EXPRESSION ; E3 LIGASE ; HYPOXIA ; VHL ; UBIQUITINATION ; DEGRADATION
Funding Organization973 Grant [2010CB126306]; National Natural Science Foundation of China [31071212, 91019008]; Chinese Academy of Sciences Major Scientific and Technological Project [XDA08010208] ; 973 Grant [2010CB126306]; National Natural Science Foundation of China [31071212, 91019008]; Chinese Academy of Sciences Major Scientific and Technological Project [XDA08010208] ; 973 Grant [2010CB126306]; National Natural Science Foundation of China [31071212, 91019008]; Chinese Academy of Sciences Major Scientific and Technological Project [XDA08010208] ; 973 Grant [2010CB126306]; National Natural Science Foundation of China [31071212, 91019008]; Chinese Academy of Sciences Major Scientific and Technological Project [XDA08010208]
Citation statistics
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/342005/20096
Collection水生生物分子与细胞生物学研究中心_期刊论文
Corresponding AuthorXiao, WH (reprint author), Chinese Acad Sci, Inst Hydrobiol, Wuhan 430072, Peoples R China.
AffiliationChinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan 430072, Peoples R China
Recommended Citation
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, WH .(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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