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Article: SOX9 elevation in the prostate promotes proliferation and cooperates with PTEN loss to drive tumor formation

TitleSOX9 elevation in the prostate promotes proliferation and cooperates with PTEN loss to drive tumor formation
Authors
Issue Date2010
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2010, v. 70 n. 3, p. 979-987 How to Cite?
AbstractDysregulation of tissue development pathways can contribute to cancer initiation and progression. In murine embryonic prostate epithelia, the transcription factor SOX9 is required for proper prostate development. In this study, we examined a role for SOX9 in prostate cancer in mouse and human. In Pten and Nkx3.1 mutant mice, cells with increased levels of SOX9 appeared within prostate epithelia at early stages of neoplasia, and higher expression correlated with progression at all stages of disease. In transgenic mice, SOX9 overexpression in prostate epithelia increased cell proliferation without inducing hyperplasia. In transgenic mice that were also heterozygous for mutant Pten, SOX9 overexpression quickened the induction of high-grade prostate intraepithelial neoplasia. In contrast, Sox9 attenuation led to a decrease proliferating prostate epithelia cells in normal and homozygous Pten mutant mice with prostate neoplasia. Analysis of a cohort of 880 human prostate cancer samples showed that SOX9 expression was associated with increasing Gleason grades and higher Ki67 staining. Our findings identify SOX9 as part of a developmental pathway that is reactivated in prostate neoplasia where it promotes tumor cell proliferation. ©2010 AACR.
Persistent Identifierhttp://hdl.handle.net/10722/96400
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
Funding AgencyGrant Number
The Orchid Appeal
Research Grants Council of Hong KongHKU7337/01M
HKU2/02C
AoE/M-04/04
National Cancer Research Institute
Funding Information:

The Orchid Appeal (D.M. Berney); the Research Grants Council of Hong Kong, grants HKU7337/01M, HKU2/02C, and AoE/M-04/04 (K.S.E. Cheah and S. Wynn); and the National Cancer Research Institute.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorThomsen, MKen_HK
dc.contributor.authorAmbroisine, Len_HK
dc.contributor.authorWynn, Sen_HK
dc.contributor.authorCheah, KSEen_HK
dc.contributor.authorFoster, CSen_HK
dc.contributor.authorFisher, Gen_HK
dc.contributor.authorBerney, DMen_HK
dc.contributor.authorMøller, Hen_HK
dc.contributor.authorReuter, VEen_HK
dc.contributor.authorScardino, Pen_HK
dc.contributor.authorCuzick, Jen_HK
dc.contributor.authorRagavan, Nen_HK
dc.contributor.authorSingh, PBen_HK
dc.contributor.authorMartin, FLen_HK
dc.contributor.authorButler, CMen_HK
dc.contributor.authorCooper, CSen_HK
dc.contributor.authorSwain, Aen_HK
dc.contributor.authorTransatlantic Prostate Group-
dc.date.accessioned2010-09-25T16:32:38Z-
dc.date.available2010-09-25T16:32:38Z-
dc.date.issued2010en_HK
dc.identifier.citationCancer Research, 2010, v. 70 n. 3, p. 979-987en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/96400-
dc.description.abstractDysregulation of tissue development pathways can contribute to cancer initiation and progression. In murine embryonic prostate epithelia, the transcription factor SOX9 is required for proper prostate development. In this study, we examined a role for SOX9 in prostate cancer in mouse and human. In Pten and Nkx3.1 mutant mice, cells with increased levels of SOX9 appeared within prostate epithelia at early stages of neoplasia, and higher expression correlated with progression at all stages of disease. In transgenic mice, SOX9 overexpression in prostate epithelia increased cell proliferation without inducing hyperplasia. In transgenic mice that were also heterozygous for mutant Pten, SOX9 overexpression quickened the induction of high-grade prostate intraepithelial neoplasia. In contrast, Sox9 attenuation led to a decrease proliferating prostate epithelia cells in normal and homozygous Pten mutant mice with prostate neoplasia. Analysis of a cohort of 880 human prostate cancer samples showed that SOX9 expression was associated with increasing Gleason grades and higher Ki67 staining. Our findings identify SOX9 as part of a developmental pathway that is reactivated in prostate neoplasia where it promotes tumor cell proliferation. ©2010 AACR.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshEpithelium - metabolism - pathologyen_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHomeodomain Proteins - genetics - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshKaplan-Meier Estimateen_HK
dc.subject.meshKi-67 Antigen - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshPTEN Phosphohydrolase - genetics - metabolismen_HK
dc.subject.meshProstate - metabolism - pathologyen_HK
dc.subject.meshProstatic Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSOX9 Transcription Factor - genetics - metabolismen_HK
dc.subject.meshTissue Array Analysisen_HK
dc.subject.meshTranscription Factors - genetics - metabolismen_HK
dc.titleSOX9 elevation in the prostate promotes proliferation and cooperates with PTEN loss to drive tumor formationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-5472&volume=70&issue=3&spage=979&epage=87&date=2010&atitle=SOX9+elevation+in+the+prostate+promotes+proliferation+and+cooperates+with+PTEN+loss+to+drive+tumor+formation.en_HK
dc.identifier.emailCheah, KSE:hrmbdkc@hku.hken_HK
dc.identifier.authorityCheah, KSE=rp00342en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-09-2370en_HK
dc.identifier.pmid20103652-
dc.identifier.scopuseid_2-s2.0-76249098305en_HK
dc.identifier.hkuros169178en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-76249098305&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume70en_HK
dc.identifier.issue3en_HK
dc.identifier.spage979en_HK
dc.identifier.epage987en_HK
dc.identifier.isiWOS:000278485600015-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectDevelopmental genomics and skeletal research-
dc.identifier.scopusauthoridThomsen, MK=37021081900en_HK
dc.identifier.scopusauthoridAmbroisine, L=34567522600en_HK
dc.identifier.scopusauthoridWynn, S=36464623600en_HK
dc.identifier.scopusauthoridCheah, KSE=35387746200en_HK
dc.identifier.scopusauthoridFoster, CS=34770077700en_HK
dc.identifier.scopusauthoridFisher, G=7402439941en_HK
dc.identifier.scopusauthoridBerney, DM=6701628860en_HK
dc.identifier.scopusauthoridMøller, H=14045738400en_HK
dc.identifier.scopusauthoridReuter, VE=7102568582en_HK
dc.identifier.scopusauthoridScardino, P=7102946217en_HK
dc.identifier.scopusauthoridCuzick, J=7103156622en_HK
dc.identifier.scopusauthoridRagavan, N=13105545000en_HK
dc.identifier.scopusauthoridSingh, PB=35727915400en_HK
dc.identifier.scopusauthoridMartin, FL=35499736700en_HK
dc.identifier.scopusauthoridButler, CM=7201550896en_HK
dc.identifier.scopusauthoridCooper, CS=7403318830en_HK
dc.identifier.scopusauthoridSwain, A=7103180047en_HK
dc.customcontrol.immutablesml 140604-

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