English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/180560
Share/Impact:
Statistics
logo share SHARE   Add this article to your Mendeley library MendeleyBASE
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE
Exportar a otros formatos:

DC FieldValueLanguage
dc.contributor.authorMartín-Pérez, Rosaes_ES
dc.contributor.authorYerbes, Rosarioes_ES
dc.contributor.authorMora-Molina, Rocíoes_ES
dc.contributor.authorCano-González, Anaes_ES
dc.contributor.authorArribas, Joaquínes_ES
dc.contributor.authorMazzone, Massimilianoes_ES
dc.contributor.authorLópez-Rivas, Abelardoes_ES
dc.contributor.authorPalacios, Carmen-
dc.date.accessioned2019-04-25T11:31:06Z-
dc.date.available2019-04-25T11:31:06Z-
dc.date.issued2018-05-06-
dc.identifier.citation11th European Workshop on Cell Death (2018)es_ES
dc.identifier.urihttp://hdl.handle.net/10261/180560-
dc.descriptionTrabajo presentado en el 11th European Workshop on Cell Death, celebrado en Fiuggi (Italia), del 6 al 11 de mayo de 2018es_ES
dc.description.abstractOncogenic transformation triggers reprogramming of cell metabolism, as part of the tumorigenic process. However, metabolic reprogramming may also increase the sensitivity of transformed cells to microenvironmental stress, at the early stages of tumor development. Herein, we show that transformation of human breast epithelial cells by the p95HER2/611CTF oncogene markedly sensitizes these cells to metabolic stress induced by the simultaneous inhibition of glucose and glutamine metabolism. In p95HER2/611CTF-transformed cells, metabolic stress activates a TNF related apoptosis-inducing ligand (TRAIL)-R and caspase-8-dependent apoptotic process that requires prior down-regulation of cellular FLICE-like inhibitor protein (c-FLIP) levels. Importantly, sustained mTOR activation is involved in FLIP down-regulation and apoptosis induced by metabolic stress. In vivo experiments in immunodeficient mice demonstrate a requirement for caspase-8 in restraining primary tumor growth of xenografts with p95HER2/611CTF-transformed cells. Collectively, these data define a critical role of the extrinsic pathway of apoptosis in the control of tumor initiation by microenvironmental cues.es_ES
dc.language.isoenges_ES
dc.rightsclosedAccesses_ES
dc.titleOncogenic p95HER2/611CTF primes human breast epithelial cells for metabolic stress-induced down-regulation of FLIP and activation of TRAIL-R/Caspase-8-dependent apoptosises_ES
dc.typecomunicación de congresoes_ES
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
Appears in Collections:(CABIMER) Comunicaciones congresos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
View/Open
Show simple item record
 


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.