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dc.contributor.authorSáez Martínez, Prudencio
dc.contributor.authorJiménez-Vacas, J.M.
dc.contributor.authorLeón González, A.J.
dc.contributor.authorHerrero-Aguayo, V.
dc.contributor.authorMontero-Hidalgo, Antonio J.
dc.contributor.authorGómez-Gómez, E.
dc.contributor.authorSánchez-Sánchez, Rafael
dc.contributor.authorRequena-Tapia, M.J.
dc.contributor.authorCastaño, Justo P.
dc.contributor.authorGahete Ortiz, Manuel D.
dc.contributor.authorLuque, Raúl M.
dc.date.accessioned2020-06-02T13:11:16Z
dc.date.available2020-06-02T13:11:16Z
dc.date.issued2020
dc.identifier.urihttp://hdl.handle.net/10396/20071
dc.description.abstractCertain components of the somatostatin-system play relevant roles in Prostate Cancer (PCa), whose most aggressive phenotype (Castration-Resistant-PCa (CRPC)) remains lethal nowadays. However, neuronostatin and the G protein-coupled receptor 107 (GPR107), two novel members of the somatostatin-system, have not been explored yet in PCa. Consequently, we investigated the pathophysiological role of NST/GPR107-system in PCa. GPR107 expression was analyzed in well-characterized PCa patient′s cohorts, and functional/mechanistic assays were performed in response to GPR107-silencing and NST-treatment in PCa cells (androgen-dependent (AD: LNCaP) and androgen-independent (AI: 22Rv1/PC-3), which are cell models of hormone-sensitive and CRPC, respectively), and normal prostate cells (RWPE-1 cell-line). GPR107 was overexpressed in PCa and associated with key clinical parameters (e.g., advance stage of PCa, presence of vascular invasion and metastasis). Furthermore, GPR107-silencing inhibited proliferation/migration rates in AI-PCa-cells and altered key genes and oncogenic signaling-pathways involved in PCa aggressiveness (i.e., KI67/CDKN2D/MMP9/PRPF40A, SST5TMD4/AR-v7/In1-ghrelin/EZH2 splicing-variants and AKT-signaling). Interestingly, NST treatment inhibited proliferation/migration only in AI-PCa cells and evoked an identical molecular response than GPR107-silencing. Finally, NST decreased GPR107 expression exclusively in AI-PCa-cells, suggesting that part of the specific antitumor effects of NST could be mediated through a GPR107-downregulation. Altogether, NST/GPR107-system could represent a valuable diagnostic and prognostic tool and a promising novel therapeutic target for PCa and CRPC.es_ES
dc.format.mimetypeapplication/pdfes_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rightshttps://creativecommons.org/licenses/by/4.0/es_ES
dc.sourceJournal of Clinical Medicine 9(6), 1703 (2020)es_ES
dc.subjectProstate canceres_ES
dc.subjectCastration resistant prostate canceres_ES
dc.subjectNeuronostatines_ES
dc.subjectG protein‐coupled receptor GPR107es_ES
dc.subjectDiagnostic/prognostic biomarkeres_ES
dc.subjectTherapeutic targetes_ES
dc.subjectSomatostatin‐systemes_ES
dc.subjectSplicinges_ES
dc.titleUnleashing the Diagnostic, Prognostic and Therapeutic Potential of the Neuronostatin/GPR107 System in Prostate Canceres_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherversionhttp://dx.doi.org/10.3390/jcm9061703es_ES
dc.relation.projectIDInstituto de Salud Carlos III. PI16/00264es_ES
dc.relation.projectIDInstituto de Salud Carlos III. PI17/02287es_ES
dc.relation.projectIDInstituto de Salud Carlos III. CD16/00092es_ES
dc.relation.projectIDGobierno de España. FPU17/00263es_ES
dc.relation.projectIDGobierno de España. FPU16/06190es_ES
dc.relation.projectIDGobierno de España. FPU18/02485es_ES
dc.relation.projectIDGobierno de España.  BFU2016‐80360‐Res_ES
dc.relation.projectIDJunta de Andalucía. BIO‐0139es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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