Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/56145
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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-
dc.date.accessioned2022-11-24T10:49:19Z-
dc.date.available2022-11-24T10:49:19Z-
dc.date.issued2019-11-01-
dc.identifier.citationBueno MJ, Jimenez-Renard V, Samino S, Capellades J, Junza A, López-Rodríguez ML, Garcia-Carceles J, Lopez-Fabuel I, Bolaños JP, Chandel NS, Yanes O, Colomer R, Quintela-Fandino M. Essentiality of fatty acid synthase in the 2D to anchorage-independent growth transition in transforming cells. Nat Commun. 2019 Nov 1;10(1):5011. doi: 10.1038/s41467-019-13028-1. PMID: 31676791; PMCID: PMC6825217.es_ES
dc.identifier.issn2041-1723-
dc.identifier.urihttps://hdl.handle.net/20.500.12530/56145-
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 Economía 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 León (Escalera de Excelencia CLU-2017-03), Ayudas Equipos Investigación Biomedicina 2017 Fundación BBVA, and Fundación Ramón Areces. This study was partially supported by the generous donations from Fundación CRIS Contra el Cáncer and AVON Spain.es_ES
dc.language.isoenes_ES
dc.publisherSpringer Science and Business Media LLCes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rightsAtribución 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subject.meshAnimalses_ES
dc.subject.meshCell Linees_ES
dc.subject.meshCells, Culturedes_ES
dc.subject.meshEmbryo, Mammalianes_ES
dc.subject.meshEmbryonic Stem Cellses_ES
dc.subject.meshFatty Acid Synthaseses_ES
dc.subject.meshFatty Acidses_ES
dc.subject.meshFemalees_ES
dc.subject.meshFibroblastses_ES
dc.subject.meshHEK293 Cellses_ES
dc.subject.meshHumanses_ES
dc.subject.meshMalees_ES
dc.subject.meshMice, Inbred C57BLes_ES
dc.subject.meshMice, Knockoutes_ES
dc.subject.meshMice, Nudees_ES
dc.subject.meshMice, Transgenices_ES
dc.subject.meshNeoplasms, Experimentales_ES
dc.subject.meshTumor Burdenes_ES
dc.titleEssentiality of fatty acid synthase in the 2D to anchorage-independent growth transition in transforming cellses_ES
dc.typeArtículoes_ES
dc.identifier.pubmedID31676791es_ES
dc.format.volume10es_ES
dc.format.page5011es_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.contributor.funderEuropean Regional Development Fund (ERDF)es_ES
dc.contributor.funderAsociación Española contra el Cánceres_ES
dc.contributor.funderMinisterio de Sanidades_ES
dc.contributor.funderNational Institute of Healthes_ES
dc.contributor.funderMinisterio de Economía y Competitividades_ES
dc.contributor.funderJunta de Castilla y Leónes_ES
dc.contributor.funderFundación BBVAes_ES
dc.contributor.funderFundación Areceses_ES
dc.contributor.funderFundación CRIS Contra el Cánceres_ES
dc.contributor.funderAVON Spaines_ES
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1038/s41467-019-13028-1es_ES
dc.identifier.journalNature communicationses_ES
dc.identifier.journalabbreviationNat Communes_ES
dc.contributor.authoraffiliationServicio de Oncología Médica. Hospital Universitario de Fuenlabradaes_ES
dc.format.number1es_ES
dc.subject.decsLínea Celulares_ES
dc.subject.decsCélulas Cultivadases_ES
dc.subject.decsEmbrión de Mamíferoses_ES
dc.subject.decsCélulas Madre Embrionariases_ES
dc.subject.decsÁcidos Grasoses_ES
dc.subject.decsFibroblastoses_ES
dc.subject.decsCélulas HEK293es_ES
dc.subject.decsCarga Tumorales_ES
dc.subject.decsNeoplasias Experimentaleses_ES
Appears in Collections:Hospitales > H. U. de Fuenlabrada > Artículos

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