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RAC1b overexpression stimulates proliferation and NF-kB-mediated anti-apoptotic signaling in thyroid cancer cells

2017-02-24Journal article Open access
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dc.contributor.authorFaria, Márcia
dc.contributor.authorMatos, Paulo
dc.contributor.authorPereira, Teresa
dc.contributor.authorCabrera, Rafael
dc.contributor.authorCardoso, Bruno A.
dc.contributor.authorBugalho, Maria João
dc.contributor.authorSilva, Ana Luísa
dc.date.accessioned2018-03-22T19:09:09Z
dc.date.available2018-03-22T19:09:09Z
dc.date.issued2017-02-24
dc.description.abstractOverexpression of tumor-associated RAC1b has been recently highlighted as one of the most promising targets for therapeutic intervention in colon, breast, lung and pancreatic cancer. RAC1b is a hyperactive variant of the small GTPase RAC1 and has been recently shown to be overexpressed in a subset of papillary thyroid carcinomas associated with unfavorable outcome. Using the K1 PTC derived cell line as an in vitro model, we observed that both RAC1 and RAC1b were able to induce a significant increase on NF-kB and cyclin D1 reporter activity. A clear p65 nuclear localization was found in cells transfected with RAC1b-WT, confirming NF-kB canonical pathway activation. Consistently, we observed a RAC1b-mediated decrease in IκBα (NF-kB inhibitor) protein levels. Moreover, we show that RAC1b overexpression stimulates G1/S progression and protects thyroid cells against induced apoptosis, the latter through a process involving the NF-kB pathway. Present data support previous findings suggesting an important role for RAC1b in the development of follicular cell-derived thyroid malignancies and point out NF-kB activation as one of the molecular mechanisms associated with the pro-tumorigenic advantage of RAC1b overexpression in thyroid carcinomas.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationPLoS One. 2017 Feb 24;12(2):e0172689. doi: 10.1371/journal.pone.0172689. eCollection 2017.pt_PT
dc.identifier.doi10.1371/journal.pone.0172689pt_PT
dc.identifier.issn1932-6203)
dc.identifier.urihttp://hdl.handle.net/10400.18/5458
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherPublic Library of Sciencept_PT
dc.relation.publisherversionhttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0172689pt_PT
dc.subjectApoptosispt_PT
dc.subjectCell Line, Tumorpt_PT
dc.subjectCell Proliferationpt_PT
dc.subjectCyclin D1pt_PT
dc.subjectG1 Phase Cell Cycle Checkpointspt_PT
dc.subjectHumanspt_PT
dc.subjectNF-KappaB Inhibitor alphapt_PT
dc.subjectNF-kappa Bpt_PT
dc.subjectSignal Transductionpt_PT
dc.subjectStaurosporinept_PT
dc.subjectThyroid Epithelial Cellspt_PT
dc.subjectTransfectionpt_PT
dc.subjectrac1 GTP-Binding Proteinpt_PT
dc.subjectGene Expression Regulation, Neoplasticpt_PT
dc.subjectVias de Transdução de Sinal e Patologias Associadaspt_PT
dc.titleRAC1b overexpression stimulates proliferation and NF-kB-mediated anti-apoptotic signaling in thyroid cancer cellspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue2pt_PT
oaire.citation.startPagee0172689pt_PT
oaire.citation.titlePLoS Onept_PT
oaire.citation.volume12pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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