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dc.contributor.authorAguilar-Morante, Dianaen_US
dc.contributor.authorMorales-Garcia, Jose Angelen_US
dc.contributor.authorSanz-SanCristobal, Marinaen_US
dc.contributor.authorGarcia-Cabezas, Miguel Angelen_US
dc.contributor.authorSantos, Angelen_US
dc.contributor.authorPerez-Castillo, Anaen_US
dc.coverage.spatialUnited Statesen_US
dc.date2010-10-19
dc.date.accessioned2018-05-14T16:59:02Z
dc.date.available2018-05-14T16:59:02Z
dc.date.issued2010-11-08
dc.identifierhttps://www.ncbi.nlm.nih.gov/pubmed/21079728
dc.identifier.citationDiana Aguilar-Morante, Jose Angel Morales-Garcia, Marina Sanz-SanCristobal, Miguel Angel Garcia-Cabezas, Angel Santos, Ana Perez-Castillo. 2010. "Inhibition of glioblastoma growth by the thiadiazolidinone compound TDZD-8.." PLoS One, Volume 5, Issue 11:e13879?.
dc.identifier.issn1932-6203
dc.identifier.urihttps://hdl.handle.net/2144/28908
dc.description.abstractBACKGROUND: Thiadiazolidinones (TDZD) are small heterocyclic compounds first described as non-ATP competitive inhibitors of glycogen synthase kinase 3β (GSK-3β). In this study, we analyzed the effects of 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8), on murine GL261 cells growth in vitro and on the growth of established intracerebral murine gliomas in vivo. METHODOLOGY/PRINCIPAL FINDINGS: Our data show that TDZD-8 decreased proliferation and induced apoptosis of GL261 glioblastoma cells in vitro, delayed tumor growth in vivo, and augmented animal survival. These effects were associated with an early activation of extracellular signal-regulated kinase (ERK) pathway and increased expression of EGR-1 and p21 genes. Also, we observed a sustained activation of the ERK pathway, a concomitant phosphorylation and activation of ribosomal S6 kinase (p90RSK) and an inactivation of GSK-3β by phosphorylation at Ser 9. Finally, treatment of glioblastoma stem cells with TDZD-8 resulted in an inhibition of proliferation and self-renewal of these cells. CONCLUSIONS/SIGNIFICANCE: Our results suggest that TDZD-8 uses a novel mechanism to target glioblastoma cells, and that malignant progenitor population could be a target of this compound.en_US
dc.format.extente13879en_US
dc.languageeng
dc.relation.ispartofPLoS One
dc.rightsCopyright: © 2010 Aguilar-Morante et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectAnimalsen_US
dc.subjectApoptosisen_US
dc.subjectCaspase 2en_US
dc.subjectCell line, tumoren_US
dc.subjectCell proliferationen_US
dc.subjectCell survivalen_US
dc.subjectGlioblastomaen_US
dc.subjectGlycogen synthase kinase 3en_US
dc.subjectGlycogen synthase kinase 3 betaen_US
dc.subjectHumansen_US
dc.subjectImmunoblottingen_US
dc.subjectImmunohistochemistryen_US
dc.subjectMAP kinase signaling systemen_US
dc.subjectMaleen_US
dc.subjectMiceen_US
dc.subjectMice, inbred C57BLen_US
dc.subjectMitogen-activated protein kinasesen_US
dc.subjectNF-kappa Ben_US
dc.subjectNeoplasm transplantationen_US
dc.subjectPhosphorylationen_US
dc.subjectProliferating cell nuclear antigenen_US
dc.subjectThiadiazolesen_US
dc.subjectTransplantation, homologousen_US
dc.subjectTumor burdenen_US
dc.titleInhibition of glioblastoma growth by the thiadiazolidinone compound TDZD-8en_US
dc.typeArticleen_US
dc.identifier.doi10.1371/journal.pone.0013879
pubs.elements-sourcepubmeden_US
pubs.notesEmbargo: No embargoen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Health & Rehabilitation Sciences: Sargent Collegeen_US
pubs.organisational-groupBoston University, College of Health & Rehabilitation Sciences: Sargent College, Health Sciencesen_US
pubs.publication-statusPublished onlineen_US
dc.identifier.orcid0000-0003-0534-5182 (Garcia-Cabezas, Miguel Angel)


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Copyright: © 2010 Aguilar-Morante et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright: © 2010 Aguilar-Morante et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.