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dc.contributor.authorAguilar Morante, Diana-
dc.contributor.authorCortés-Canteli, Marta-
dc.contributor.authorSanz-SanCristóbal, Marina-
dc.contributor.authorPérez Castillo, Ana-
dc.contributor.authorSantos, Ángel-
dc.date.accessioned2013-05-23T13:00:10Z-
dc.date.available2013-05-23T13:00:10Z-
dc.date.issued2011-
dc.identifierdoi: 10.1016/j.neuroscience.2010.12.025-
dc.identifierissn: 0306-4522-
dc.identifiere-issn: 1873-7544-
dc.identifier.citationNeuroscience 176: 110-119 (2011)-
dc.identifier.urihttp://hdl.handle.net/10261/76671-
dc.description.abstractC/EBPβ is a leucine-zipper transcription factor implicated in the control of metabolism, development, cell differentiation, and proliferation. However, it remains unclear its role in tumor development. Here, we show that down-regulation of C/EBPβ by RNA interference inhibits proliferation in the GL261 murine glioblastoma cell line, induces an arrest of the cell cycle at the G0/G1 boundary, and diminishes their transformation capacity and migration. In addition, we show that C/EBPβ regulates the expression of several DNA damage response- and invasion-related genes. Lastly, C/EBPβ depletion significantly retards tumor onset and prolongs survival in a murine orthotopic brain tumor model. Immunohistochemical analysis revealed a significant diminution of proliferating cell nuclear antigen (PCNA) labeling in tumors derived from C/EBPβ-depleted GL261 cells compared with that in controls. These results show, for the first time, the dependence of glioma cells on C/EBPβ and suggest a potential role of this transcription factor in glioma development. © 2011 IBRO.-
dc.description.sponsorshipThis work was supported by the Ministerio de Educacion y Ciencia grant SAF2007-62811 (to A.P.-C). CIBERNED is founded by the Instituto de Salud Carlos III. D.A.-M is a fellow of the Consejo Superior de Investigaciones Científicas.-
dc.language.isoeng-
dc.publisherElsevier-
dc.rightsopenAccess-
dc.titleDecreased CCAAT/enhancer binding protein β expression inhibits the growth of glioblastoma cells-
dc.typeartículo-
dc.identifier.doi10.1016/j.neuroscience.2010.12.025-
dc.relation.publisherversionhttp://dx.doi.org/10.1016/j.neuroscience.2010.12.025-
dc.date.updated2013-05-23T13:00:10Z-
dc.description.versionPeer Reviewed-
dc.contributor.funderMinisterio de Educación y Ciencia (España)-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderConsejo Superior de Investigaciones Científicas (España)-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003339es_ES
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