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Article: Orphan nuclear receptor estrogen-related receptor-β suppresses in vitro and in vivo growth of prostate cancer cells via p21WAF1/CIP1 induction and as a potential therapeutic target in prostate cancer

TitleOrphan nuclear receptor estrogen-related receptor-β suppresses in vitro and in vivo growth of prostate cancer cells via p21WAF1/CIP1 induction and as a potential therapeutic target in prostate cancer
Authors
Issue Date2008
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2008, v. 27 n. 23, p. 3313-3328 How to Cite?
AbstractRecent studies indicate that estrogen-related receptors (ERRs) are involved in similar estrogen receptor (ER) regulatory pathways and play roles in energy and lipid metabolism. Here, we analysed the functional role of ERRβ in prostate cancer cell growth regulation in an androgen-sensitive and androgen-insensitive prostate cancer cell lines. ERRβ was expressed in normal human prostates, but exhibited a reduced expression in prostate cancer lesions. Stable ERRβ expression suppressed significantly cell proliferation and tumorigenicity of LNCaP and DU145 cells, accompanied by an S-phase suppression and increased p21 expression. Reporter and chromatin immunoprecipitation assays showed that ERRβ could directly transactivate p21 gene promoter, which could be further enhanced by peroxisome proliferator-activated receptor-γ coactivator-1α. Truncation analysis showed that ERRβ-mediated p21 transactivation and prostate cancer cell growth inhibition required intact DNA-binding domain and AF2 domains in ERRβ. Interestingly, ERRβ displayed a cell cycle associated downregulated expression pattern in ERRβ-transduced and non-transduced cells. Finally, we showed that ERRβ-mediated growth inhibition could be potentiated by an ERRβ/γ agonist DY131. Knockdown of ERRβ by RNA interference could reduce the DY131-induced growth inhibition in prostate cancer cells. Taken together, our findings indicate that ERRβ performs a tumor suppressing function in prostate cancer cells, and targeting ERRβ could be a potential therapeutic strategy for prostate cancer. © 2008 Nature Publishing Group All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/149695
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYu, Sen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorWang, XHen_US
dc.contributor.authorLing, MTen_US
dc.contributor.authorNg, CFen_US
dc.contributor.authorChen, Sen_US
dc.contributor.authorChan, FLen_US
dc.date.accessioned2012-06-26T05:57:12Z-
dc.date.available2012-06-26T05:57:12Z-
dc.date.issued2008en_US
dc.identifier.citationOncogene, 2008, v. 27 n. 23, p. 3313-3328en_US
dc.identifier.issn0950-9232en_US
dc.identifier.urihttp://hdl.handle.net/10722/149695-
dc.description.abstractRecent studies indicate that estrogen-related receptors (ERRs) are involved in similar estrogen receptor (ER) regulatory pathways and play roles in energy and lipid metabolism. Here, we analysed the functional role of ERRβ in prostate cancer cell growth regulation in an androgen-sensitive and androgen-insensitive prostate cancer cell lines. ERRβ was expressed in normal human prostates, but exhibited a reduced expression in prostate cancer lesions. Stable ERRβ expression suppressed significantly cell proliferation and tumorigenicity of LNCaP and DU145 cells, accompanied by an S-phase suppression and increased p21 expression. Reporter and chromatin immunoprecipitation assays showed that ERRβ could directly transactivate p21 gene promoter, which could be further enhanced by peroxisome proliferator-activated receptor-γ coactivator-1α. Truncation analysis showed that ERRβ-mediated p21 transactivation and prostate cancer cell growth inhibition required intact DNA-binding domain and AF2 domains in ERRβ. Interestingly, ERRβ displayed a cell cycle associated downregulated expression pattern in ERRβ-transduced and non-transduced cells. Finally, we showed that ERRβ-mediated growth inhibition could be potentiated by an ERRβ/γ agonist DY131. Knockdown of ERRβ by RNA interference could reduce the DY131-induced growth inhibition in prostate cancer cells. Taken together, our findings indicate that ERRβ performs a tumor suppressing function in prostate cancer cells, and targeting ERRβ could be a potential therapeutic strategy for prostate cancer. © 2008 Nature Publishing Group All rights reserved.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_US
dc.relation.ispartofOncogeneen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntineoplastic Agents - Therapeutic Useen_US
dc.subject.meshCarcinoma - Drug Therapy - Genetics - Pathologyen_US
dc.subject.meshCell Cycle - Geneticsen_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P21 - Geneticsen_US
dc.subject.meshDrug Delivery Systemsen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshHela Cellsen_US
dc.subject.meshHeat-Shock Proteins - Physiologyen_US
dc.subject.meshHistone Deacetylases - Metabolismen_US
dc.subject.meshHistones - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Sciden_US
dc.subject.meshProstatic Neoplasms - Drug Therapy - Genetics - Pathologyen_US
dc.subject.meshProtein Structure, Tertiary - Physiologyen_US
dc.subject.meshReceptors, Estrogen - Agonists - Chemistry - Genetics - Physiologyen_US
dc.subject.meshTranscription Factors - Physiologyen_US
dc.subject.meshTransfectionen_US
dc.subject.meshTransplantation, Heterologousen_US
dc.subject.meshUp-Regulationen_US
dc.titleOrphan nuclear receptor estrogen-related receptor-β suppresses in vitro and in vivo growth of prostate cancer cells via p21WAF1/CIP1 induction and as a potential therapeutic target in prostate canceren_US
dc.typeArticleen_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.identifier.authorityLing, MT=rp00449en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.onc.1210986en_US
dc.identifier.pmid18071305-
dc.identifier.scopuseid_2-s2.0-44349192262en_US
dc.identifier.hkuros147808-
dc.identifier.hkuros147321-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-44349192262&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume27en_US
dc.identifier.issue23en_US
dc.identifier.spage3313en_US
dc.identifier.epage3328en_US
dc.identifier.isiWOS:000256111400010-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridYu, S=7405730221en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridWang, XH=7501854829en_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridNg, CF=8519137200en_US
dc.identifier.scopusauthoridChen, S=7410248480en_US
dc.identifier.scopusauthoridChan, FL=7202586505en_US
dc.identifier.citeulike2088149-

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