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dc.contributor.authorPalacios, Carmen-
dc.contributor.authorLópez-Pérez, Ana Isabel-
dc.contributor.authorLópez-Rivas, Abelardo-
dc.date.accessioned2011-08-12T07:12:49Z-
dc.date.available2011-08-12T07:12:49Z-
dc.date.issued2010-01-
dc.identifier.citationCancer Letters 287(2): 207-215 (2010)es_ES
dc.identifier.issn0304-3835-
dc.identifier.urihttp://hdl.handle.net/10261/38666-
dc.description9 páginas, 4 figuras.es_ES
dc.description.abstractThe Hsp90 inhibitor 17DMAG (17-dimethylaminoethylamino-17-demethoxygeldanamycin) is undergoing clinical trials as an antitumor drug. We show here that treatment of human breast cancer cells with 17DMAG facilitates tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Down-regulation of receptor interacting protein (RIP1) is observed upon 17DMAG treatment concomitantly with inhibition of IκBα phosphorylation. Interestingly, RNAi-mediated knockdown of RIP1 expression is sufficient to sensitize human breast tumor cells to TRAIL-induced apoptosis through a NF-κB-independent, mitochondria-operated pathway. Our results indicate that RIP1 is important in maintaining resistance to TRAIL-induced apoptosis in breast tumor cells and highlight the potential therapeutic benefit of the combination of Hsp90 inhibitors and TRAIL against breast tumor cells.es_ES
dc.description.sponsorshipThis work was supported by grants from Ministerio de Educación y Ciencia (SAF2006-00633), Red Temática de Investigación Cooperativa en Cáncer (RTICC) (RD06/0020/ 0068) and Junta de Andalucía (CTS-211) to ALR. CP and AILP were supported by contracts from Junta de Andalucía and Ministerio de Ciencia e Innovación, respectively.es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.rightsclosedAccesses_ES
dc.subject17DMAGes_ES
dc.subjectTRAILes_ES
dc.subjectApoptosises_ES
dc.subjectRIP1es_ES
dc.titleDown-regulation of RIP expression by 17-dimethylaminoethylamino-17-demethoxygeldanamycin promotes TRAIL-induced apoptosis in breast tumor cellses_ES
dc.typeartículoes_ES
dc.identifier.doi10.1016/j.canlet.2009.06.012-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1016/j.canlet.2009.06.012es_ES
dc.contributor.funderMinisterio de Educación y Ciencia (España)-
dc.contributor.funderJunta de Andalucía-
dc.contributor.funderRed Temática de Investigación Cooperativa en Cáncer (España)-
dc.contributor.funderMinisterio de Ciencia e Innovación (España)-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004837es_ES
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