PROP1 overexpression in corticotrophinomas: evidence for the role of PROP1 in the maintenance of cells committed to corticotrophic differentiation

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorARAUJO, Ricardo V.
dc.contributor.authorCHANG, Claudia V.
dc.contributor.authorCESCATO, Valter A. S.
dc.contributor.authorFRAGOSO, Maria Candida B. V.
dc.contributor.authorBRONSTEIN, Marcello D.
dc.contributor.authorMENDONCA, Berenice B.
dc.contributor.authorARNHOLD, Ivo J. P.
dc.contributor.authorCARVALHO, Luciani R. S.
dc.date.accessioned2013-09-23T16:36:11Z
dc.date.available2013-09-23T16:36:11Z
dc.date.issued2013
dc.description.abstractOBJECTIVE: The expression of transcription factors involved in early pituitary development, such as PROP1 and POU1F1, has been detected in pituitary adenoma tissues. In this study, we sought to characterize the transcriptional profiles of PROP1, POU1F1, and TBX19 in functioning and nonfunctioning pituitary adenomas in an attempt to identify their roles in tumorigenesis and hormone hypersecretion. METHODS: RT-qPCR analyses were performed to assess the transcriptional pattern of PROP1, POU1F1, TBX19, and hormone-producing genes in tissue samples of corticotrophinomas (n = 10), somatotrophinomas (n = 8), and nonfunctioning adenomas (n = 6). RESULTS: Compared with normal pituitary tissue, POU1F1 was overexpressed in somatotrophinomas by 3-fold. PROP1 expression was 18-fold higher in corticotrophinomas, 10-fold higher in somatotrophinomas, and 3-fold higher in nonfunctioning adenomas. TBX19 expression was 27-fold higher in corticotrophinomas. Additionally, the level of TBX19 mRNA positively correlated with that of pro-opiomelanocortin (r = 0.49, p = 0.014). CONCLUSIONS: Our data demonstrate that PROP1 is overexpressed in pituitary adenomas, mainly in corticotrophinomas. Together with previously published data showing that patients who harbor PROP1 loss-of-function mutations present a progressive decline in corticotrope function, our results support a role for PROP1 in pituitary tumor development and in the maintenance of cell lineages committed to corticotrophic differentiation.
dc.description.indexMEDLINE
dc.description.sponsorshipFundacao Faculdade de Medicina (FFM)
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
dc.identifier.citationCLINICS, v.68, n.6, p.887-891, 2013
dc.identifier.doi10.6061/clinics/2013(06)26
dc.identifier.issn1807-5932
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/1780
dc.language.isoeng
dc.publisherHOSPITAL CLINICAS, UNIV SAO PAULO
dc.relation.ispartofClinics
dc.rightsopenAccess
dc.rights.holderCopyright HOSPITAL CLINICAS, UNIV SAO PAULO
dc.subjectPituitary Neoplasms
dc.subjectPROP1
dc.subjectPOU1F1
dc.subjectTBX19
dc.subject.otherpituitary-hormone deficiency
dc.subject.othergene-expression
dc.subject.otherproteomic analyses
dc.subject.otheradenomas
dc.subject.othermechanisms
dc.subject.othermutations
dc.subject.othertumors
dc.subject.otherpit-1
dc.subject.wosMedicine, General & Internal
dc.titlePROP1 overexpression in corticotrophinomas: evidence for the role of PROP1 in the maintenance of cells committed to corticotrophic differentiation
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.citation.scopus10
hcfmusp.contributor.author-fmusphcRICARDO VIEIRA ARAUJO
hcfmusp.contributor.author-fmusphcCLAUDIA VEIGA CHANG
hcfmusp.contributor.author-fmusphcVALTER ANGELO SPERLING CESCATO
hcfmusp.contributor.author-fmusphcMARIA CANDIDA BARISSON VILLARES FRAGOSO
hcfmusp.contributor.author-fmusphcMARCELLO DELANO BRONSTEIN
hcfmusp.contributor.author-fmusphcBERENICE BILHARINHO DE MENDONCA
hcfmusp.contributor.author-fmusphcIVO JORGE PRADO ARNHOLD
hcfmusp.contributor.author-fmusphcLUCIANI RENATA SILVEIRA DE CARVALHO
hcfmusp.description.beginpage887
hcfmusp.description.endpage891
hcfmusp.description.issue6
hcfmusp.description.volume68
hcfmusp.origemWOS
hcfmusp.origem.pubmed23778486
hcfmusp.origem.scieloSCIELO:S1807-59322013000600887
hcfmusp.origem.scopus2-s2.0-84879315688
hcfmusp.origem.wosWOS:000320463800026
hcfmusp.publisher.citySAO PAULO
hcfmusp.publisher.countryBRAZIL
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hcfmusp.remissive.sponsorshipFAPESP
hcfmusp.remissive.sponsorshipFFM
hcfmusp.scopus.lastupdate2024-05-17
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