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dc.contributor.authorBueno, Maria J
dc.contributor.authorJimenez-Renard, Veronica
dc.contributor.authorSamino, Sara
dc.contributor.authorCapellades, Jordi
dc.contributor.authorJunza, Alejandra
dc.contributor.authorLópez-Rodríguez, María Luz
dc.contributor.authorGarcia-Carceles, Javier
dc.contributor.authorLopez-Fabuel, Irene
dc.contributor.authorBolaños, Juan P
dc.contributor.authorChandel, Navdeep S
dc.contributor.authorYanes, Oscar
dc.contributor.authorColomer, Ramon
dc.contributor.authorQuintela Fandino, Miguel Angel 
dc.date.accessioned2020-03-24T18:31:59Z
dc.date.available2020-03-24T18:31:59Z
dc.date.issued2019-11-01
dc.identifier.citationNat Commun. 2019 ;10(1):5011es_ES
dc.identifier.issn2041-1723es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9317
dc.description.abstractUpregulation of fatty acid synthase (FASN) is a common event in cancer, although its mechanistic and potential therapeutic roles are not completely understood. In this study, we establish a key role of FASN during transformation. FASN is required for eliciting the anaplerotic shift of the Krebs cycle observed in cancer cells. However, its main role is to consume acetyl-CoA, which unlocks isocitrate dehydrogenase (IDH)-dependent reductive carboxylation, producing the reductive power necessary to quench reactive oxygen species (ROS) originated during the switch from two-dimensional (2D) to three-dimensional (3D) growth (a necessary hallmark of cancer). Upregulation of FASN elicits the 2D-to-3D switch; however, FASN's synthetic product palmitate is dispensable for this process since cells satisfy their fatty acid requirements from the media. In vivo, genetic deletion or pharmacologic inhibition of FASN before oncogenic activation prevents tumor development and invasive growth. These results render FASN as a potential target for cancer prevention studies.es_ES
dc.description.sponsorshipM.Q.F. is a recipient of the following grants: FIS PI13/00430 and FIS PI16/00354 funded by the Instituto de Salud Carlos III (ISCIII) and co-funded by the European Regional Development Fund (ERDF) and AECC Scientific Foundation (Beca de Retorno 2010). R.C. is a recipient of the following grants: FIS PI11/00832 and FIS PI14/00726 funded by the Instituto de Salud Carlos III (ISCIII) and co-funded by the European Regional Development Fund (ERDF), II14/00009 and PIE15/00068 from the Ministerio de Sanidad, Spain. N.S.C. is a recipient of an NIH grant (5R35CA197532). O.Y.T. is a recipient of the grants BFU2014-57466 from the Ministerio de Economia y Competitividad (MINECO). J.P.B. is funded by MINECO (SAF2016-78114-R), Instituto de Salud Carlos III (RD12/0043/0021), Junta de Castilla y Leon (Escalera de Excelencia CLU-2017-03), Ayudas Equipos Investigacion Biomedicina 2017 Fundacion BBVA, and Fundacion Ramon Areces. This study was partially supported by the generous donations from Fundacion CRIS Contra el Cancer and AVON Spain. We thank Drs. Erwin Wagner and Nabil Djouder for their critical review of the paper.es_ES
dc.language.isoenges_ES
dc.publisherNature Publishing Group es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshAnimals es_ES
dc.subject.meshCell Line es_ES
dc.subject.meshCells, Cultured es_ES
dc.subject.meshEmbryo, Mammalianes_ES
dc.subject.meshEmbryonic Stem Cells es_ES
dc.subject.meshFatty Acid Synthases es_ES
dc.subject.meshFatty Acids es_ES
dc.subject.meshFemale es_ES
dc.subject.meshFibroblasts es_ES
dc.subject.meshHEK293 Cells es_ES
dc.subject.meshHumans es_ES
dc.subject.meshMale es_ES
dc.subject.meshMice, Inbred C57BL es_ES
dc.subject.meshMice, Knockout es_ES
dc.subject.meshMice, Nude es_ES
dc.subject.meshMice, Transgenic es_ES
dc.subject.meshNeoplasms, Experimental es_ES
dc.subject.meshTumor Burden es_ES
dc.titleEssentiality of fatty acid synthase in the 2D to anchorage-independent growth transition in transforming cellses_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID31676791es_ES
dc.format.volume10es_ES
dc.format.number1es_ES
dc.format.page5011es_ES
dc.identifier.doi10.1038/s41467-019-13028-1es_ES
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderUnión Europea 
dc.contributor.funderAsociación Española Contra el Cáncer 
dc.contributor.funderUnited States Department of Health and Human Services 
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderJunta de Castilla y León (España) 
dc.contributor.funderFundación BBVA 
dc.contributor.funderFundación Ramón Areces 
dc.description.peerreviewedes_ES
dc.identifier.e-issn2041-1723es_ES
dc.relation.publisherversionhttps://doi.org/10.1038/s41467-019-13028-1.es_ES
dc.identifier.journalNature communicationses_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Unidades técnicas::Unidad Clínica de Cáncer Familiares_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/FIS PI13/00430es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/FIS PI16/00354es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/FIS PI11/00832es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/FIS PI14/00726es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/SAF2016-78114-Res_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/RD12/0043/0021es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/PIE15/00068es_ES
dc.rights.accessRightsopen accesses_ES


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