Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/48247
Campo DC Valoridioma
dc.contributor.authorIglesias-Gato, Diegoen_US
dc.contributor.authorChuan, Yin Choyen_US
dc.contributor.authorWikström, Pernillaen_US
dc.contributor.authorAugsten, Sandraen_US
dc.contributor.authorJiang, Ningen_US
dc.contributor.authorNiu, Yuanjieen_US
dc.contributor.authorSeipel, Amandaen_US
dc.contributor.authorDanneman, Danielaen_US
dc.contributor.authorVermeij, Marcelen_US
dc.contributor.authorFernandez-Perez, Leandroen_US
dc.contributor.authorJenster, Guidoen_US
dc.contributor.authorEgevad, Larsen_US
dc.contributor.authorNorstedt, Gunnaren_US
dc.contributor.authorFlores-Morales, Amilcaren_US
dc.date.accessioned2018-11-23T20:07:37Z-
dc.date.available2018-11-23T20:07:37Z-
dc.date.issued2014en_US
dc.identifier.issn0143-3334en_US
dc.identifier.urihttp://hdl.handle.net/10553/48247-
dc.description.abstractAnabolic signals such as androgens and the growth hormone/insulin-like growth factor 1 (GH/IGF-1) axis play an essential role in the normal development of the prostate but also in its malignant transformation. In this study, we investigated the role of suppressor of cytokine signaling 2 (SOCS2) as mediator of the cross talk between androgens and GH signals in the prostate and its potential role as tumor suppressor in prostate cancer (PCa). We observed that SOCS2 protein levels assayed by immunohistochemistry are elevated in hormone therapy-naive localized prostatic adenocarcinoma in comparison with benign tissue. In contrast, however, castration-resistant bone metastases exhibit reduced levels of SOCS2 in comparison with localized or hormone naive, untreated metastatic tumors. In PCa cells, SOCS2 expression is induced by androgens through a mechanism that requires signal transducer and activator of transcription 5 protein (STAT5) and androgen receptor-dependent transcription. Consequentially, SOCS2 inhibits GH activation of Janus kinase 2, Src and STAT5 as well as both cell invasion and cell proliferation in vitro. In vivo, SOCS2 limits proliferation and production of IGF-1 in the prostate in response to GH. Our results suggest that the use of GH-signaling inhibitors could be of value as a complementary treatment for castration-resistant PCa.Summary: Androgen induced SOCS2 ubiquitin ligase expression and inhibited GH signaling as well as cell proliferation and invasion in PCa, whereas reduced SOCS2 was present in castration-resistant cases. GH-signaling inhibitors might be a complementary therapeutic option for advanced PCa.en_US
dc.languageengen_US
dc.relation.ispartofCarcinogenesisen_US
dc.sourceCarcinogenesis[ISSN 0143-3334],v. 35, p. 24-33en_US
dc.subject32 Ciencias médicasen_US
dc.subject320101 Oncologíaen_US
dc.subject.otherGene-Expressionen_US
dc.subject.otherFactor-Ien_US
dc.subject.otherReceptor Expressionen_US
dc.subject.otherProlactinen_US
dc.subject.otherTransduceren_US
dc.subject.otherSuppressoren_US
dc.subject.otherActivatoren_US
dc.subject.otherTargeten_US
dc.subject.otherDisruptionen_US
dc.subject.otherCellsen_US
dc.titleSOCS2 mediates the cross talk between androgen and growth hormone signaling in prostate canceren_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1093/carcin/bgt304en_US
dc.identifier.scopus84891349432-
dc.identifier.isi000329130600004-
dc.contributor.authorscopusid36664682600-
dc.contributor.authorscopusid8325409300-
dc.contributor.authorscopusid7005154258-
dc.contributor.authorscopusid55979030100-
dc.contributor.authorscopusid35744765600-
dc.contributor.authorscopusid57204762630-
dc.contributor.authorscopusid24734125700-
dc.contributor.authorscopusid55602545800-
dc.contributor.authorscopusid55802115600-
dc.contributor.authorscopusid6701455114-
dc.contributor.authorscopusid6506777525-
dc.contributor.authorscopusid7004365261-
dc.contributor.authorscopusid55113533000-
dc.contributor.authorscopusid7006397634-
dc.contributor.authorscopusid57203543352-
dc.description.lastpage33en_US
dc.description.firstpage24en_US
dc.relation.volume35en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.contributor.daisngid2567702-
dc.contributor.daisngid4244439-
dc.contributor.daisngid296610-
dc.contributor.daisngid20934501-
dc.contributor.daisngid30029968-
dc.contributor.daisngid338292-
dc.contributor.daisngid3201355-
dc.contributor.daisngid3856410-
dc.contributor.daisngid803373-
dc.contributor.daisngid795544-
dc.contributor.daisngid171164-
dc.contributor.daisngid33336-
dc.contributor.daisngid178539-
dc.contributor.daisngid617657-
dc.description.numberofpages12en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Iglesias-Gato, D-
dc.contributor.wosstandardWOS:Chuan, YC-
dc.contributor.wosstandardWOS:Wikstrom, P-
dc.contributor.wosstandardWOS:Augsten, S-
dc.contributor.wosstandardWOS:Jiang, N-
dc.contributor.wosstandardWOS:Niu, YJ-
dc.contributor.wosstandardWOS:Seipel, A-
dc.contributor.wosstandardWOS:Danneman, D-
dc.contributor.wosstandardWOS:Vermeij, M-
dc.contributor.wosstandardWOS:Fernandez-Perez, L-
dc.contributor.wosstandardWOS:Jenster, G-
dc.contributor.wosstandardWOS:Egevad, L-
dc.contributor.wosstandardWOS:Norstedt, G-
dc.contributor.wosstandardWOS:Flores-Morales, A-
dc.date.coverdateEnero 2014en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr2,566-
dc.description.jcr5,334-
dc.description.sjrqQ1-
dc.description.jcrqQ1-
dc.description.scieSCIE-
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.orcid0000-0001-7802-465X-
crisitem.author.orcid0000-0002-0828-8921-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameFernández Pérez, Leandro Francisco-
crisitem.author.fullNameFlores Morales,Amilcar-
Colección:Artículos
Vista resumida

Google ScholarTM

Verifica

Altmetric


Comparte



Exporta metadatos



Los elementos en ULPGC accedaCRIS están protegidos por derechos de autor con todos los derechos reservados, a menos que se indique lo contrario.