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dc.contributor.authorBarrett, Jeffrey M.en_US
dc.contributor.authorRovedo, Mark A.en_US
dc.contributor.authorTajuddin, Aamair M.en_US
dc.contributor.authorJilling, Tamasen_US
dc.contributor.authorMacoska, Jill A.en_US
dc.contributor.authorMacDonald, Jamesen_US
dc.contributor.authorMangold, Kathy A.en_US
dc.contributor.authorKaul, Karen L.en_US
dc.date.accessioned2007-05-02T14:15:58Z
dc.date.available2007-05-02T14:15:58Z
dc.date.issued2006-05-01en_US
dc.identifier.citationBarrett, Jeffrey M.; Rovedo, Mark A.; Tajuddin, Aamair M.; Jilling, Tamas; Macoska, Jill A.; MacDonald, James; Mangold, Kathy A.; Kaul, Karen L. (2006). "Prostate cancer cells regulate growth and differentiation of bone marrow endothelial cells through TGFΒ and its receptor, TGFΒRII." The Prostate 66(6): 632-650. <http://hdl.handle.net/2027.42/50648>en_US
dc.identifier.issn0270-4137en_US
dc.identifier.issn1097-0045en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/50648
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=16388503&dopt=citationen_US
dc.description.abstractBACKGROUND The underlying mechanisms permitting prostate cancer bone metastasis are poorly understood. We previously showed that the highly metastatic prostate cancer cell line, PC-3, inhibits bone marrow endothelial (HBME-1) cell growth in collagen gels and induces them to differentiate into cords, resembling angiogenesis in vivo. METHODS cDNA microarray analysis was performed to identify cytokines responsible for the effects of PC-3 cells on HBME-1 cells. Cytokine and neutralizing antibody studies were done to further investigate specific angiogenic factors, such as transforming growth factor Β (TGFΒ). TGFΒ RNA and protein were detected by real-time RT-PCR and enzyme-linked immunosorbent assay (ELISA) analysis to measure their production by prostate cancer cell lines. Conditioned media experiments using TGFΒ neutralizing antibodies were used to analyze TGFΒ activation by prostate cancer cells. RESULTS PC-3 conditioned media altered the expression of several TGFΒ-regulated or -associated genes in HBME-1 cells. Low concentrations of TGFΒ cytokines inhibited HBME-1 cell growth to a similar level as PC-3 conditioned media and partially induced differentiation. Inhibitors and neutralizing antibodies directed against TGFΒ isoforms and TGFΒ receptor type 2 (TGFΒRII) reversed the growth inhibition of HBME-1 cells conferred by PC-3 conditioned media. Yet, only TGFΒRII neutralizing antibodies significantly inhibited HBME-1 differentiation. Also, prostate cancer cell lines produced low levels of TGFΒ RNA and protein, and were shown to activate serum-derived TGFΒ. CONCLUSIONS These results suggest that prostate cancer cells mediate growth inhibition and differentiation of bone marrow endothelial cells both through production and activation of TGFΒ as well as alteration of TGFΒRII-mediated signal transduction. This could contribute to the establishment and growth of bone metastases. Prostate 66:632–650, 2006. © 2005 Wiley-Liss, Inc.en_US
dc.format.extent251527 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherCancer Research, Oncology and Pathologyen_US
dc.titleProstate cancer cells regulate growth and differentiation of bone marrow endothelial cells through TGFΒ and its receptor, TGFΒRIIen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelInternal Medicine and Specialtiesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Urology, Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michigan ; Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumComprehensive Cancer Center, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationotherInterdepartmental Biological Sciences Program, Northwestern University, Evanston, Illinois ; Department of Pathology, Evanston Northwestern Healthcare, Evanston, Illinoisen_US
dc.contributor.affiliationotherInterdepartmental Biological Sciences Program, Northwestern University, Evanston, Illinoisen_US
dc.contributor.affiliationotherDepartment of Pathology, Evanston Northwestern Healthcare, Evanston, Illinoisen_US
dc.contributor.affiliationotherInterdepartmental Biological Sciences Program, Northwestern University, Evanston, Illinois ; Evanston Northwestern Healthcare Research Institute, Evanston, Illinoisen_US
dc.contributor.affiliationotherDepartment of Pathology, Evanston Northwestern Healthcare, Evanston, Illinoisen_US
dc.contributor.affiliationotherInterdepartmental Biological Sciences Program, Northwestern University, Evanston, Illinois ; Department of Pathology, Evanston Northwestern Healthcare, Evanston, Illinois ; Department of Urology, Northwestern University Medical School, Chicago, Illinois ; Department of Pathology, Evanston Hospital, 2650 Ridge Avenue, Evanston, IL 60201.en_US
dc.identifier.pmid16388503en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/50648/1/20370_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/pros.20370en_US
dc.identifier.sourceThe Prostateen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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