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http://hdl.handle.net/10261/188787
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dc.contributor.author | Meléndez-Rodríguez, Florinda | es_ES |
dc.contributor.author | Urrutia, Andrés A. | es_ES |
dc.contributor.author | Lorendeau, Doriane | es_ES |
dc.contributor.author | Rinaldi, Gianmarco | es_ES |
dc.contributor.author | Roche, Olga | es_ES |
dc.contributor.author | Böğürcü-Seidel, Nuray | es_ES |
dc.contributor.author | Ortega-Muelas, Marta | es_ES |
dc.contributor.author | Mesa-Ciller, Claudia | es_ES |
dc.contributor.author | Turiel, Guillermo | es_ES |
dc.contributor.author | Bouthelier, Antonio | es_ES |
dc.contributor.author | Hernansanz-Agustín, Pablo | es_ES |
dc.contributor.author | Elorza, Ainara | es_ES |
dc.contributor.author | Escasany, Elia | es_ES |
dc.contributor.author | Yang Li, Qilong Oscar | es_ES |
dc.contributor.author | Torres-Capelli, Mar | es_ES |
dc.contributor.author | Tello, Daniel | es_ES |
dc.contributor.author | Fuertes, Esther | es_ES |
dc.contributor.author | Fraga, Enrique | es_ES |
dc.contributor.author | Martínez-Ruiz, Antonio | es_ES |
dc.contributor.author | Pérez, Belén | es_ES |
dc.contributor.author | Giménez-Bachs, José M. | es_ES |
dc.contributor.author | Salinas-Sánchez, Antonio S. | es_ES |
dc.contributor.author | Acker, Till | es_ES |
dc.contributor.author | Sánchez-Prieto, Ricardo | es_ES |
dc.contributor.author | Fendt, Sarah-Maria | es_ES |
dc.contributor.author | De Bock, Katrien | es_ES |
dc.contributor.author | Aragonés, Julián | es_ES |
dc.date.accessioned | 2019-08-22T06:39:36Z | - |
dc.date.available | 2019-08-22T06:39:36Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Cell Reports 26(9): 2257-2265.e4 | es_ES |
dc.identifier.uri | http://hdl.handle.net/10261/188787 | - |
dc.description.abstract | Cellular aspartate drives cancer cell proliferation, but signaling pathways that rewire aspartate biosynthesis to control cell growth remain largely unknown. Hypoxia-inducible factor-1α (HIF1α) can suppress tumor cell proliferation. Here, we discovered that HIF1α acts as a direct repressor of aspartate biosynthesis involving the suppression of several key aspartate-producing proteins, including cytosolic glutamic-oxaloacetic transaminase-1 (GOT1) and mitochondrial GOT2. Accordingly, HIF1α suppresses aspartate production from both glutamine oxidation as well as the glutamine reductive pathway. Strikingly, the addition of aspartate to the culture medium is sufficient to relieve HIF1α-dependent repression of tumor cell proliferation. Furthermore, these key aspartate-producing players are specifically repressed in VHL-deficient human renal carcinomas, a paradigmatic tumor type in which HIF1α acts as a tumor suppressor, highlighting the in vivo relevance of these findings. In conclusion, we show that HIF1α inhibits cytosolic and mitochondrial aspartate biosynthesis and that this mechanism is the molecular basis for HIF1α tumor suppressor activity. | es_ES |
dc.description.sponsorship | This work was supported by grants from Ministerio de Economia y Competitividad (SAF2016-76815 and SAF2017-90794-REDT) and Fundació La Marató de TV3 (534/C/2016). F.M.-R. is supported by Ministerio de Economia y Competitividad (BES-2014-068618). A.A.U is supported by the CAM “Atracción de Talento” program. D.L. is supported by the VIB-Marie Curie omics program. S.-M.F. acknowledges funding support from a Marie Curie CIG, FWO Odysseus II, FWO Research Grants, Eugène Yourassowsky Schenking, and KU Leuven Methusalem co-funding. O.R. has a contract for accessing the Spanish System of Science, Technology and Innovation (SECTI) funded by the University of Castilla-La Mancha (UCLM). R.S.P acknowledges funding support from Ministerio de Educación y Ciencia (SAF2015-64215-R) and Fundacion Leticia Castillejo Castillo. A.M.-R. acknowledges funding support from Ministerio de Economía y Competitividad (PI15/00107). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Elsevier | es_ES |
dc.relation | SAF2017-90794-REDT/AEI/10.13039/501100011033 | - |
dc.relation | info:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2016-76815-R | es_ES |
dc.relation | info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/SAF2017-90794-REDT | es_ES |
dc.relation | info:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2015-64215-R | es_ES |
dc.relation.isversionof | Publisher's version | es_ES |
dc.rights | openAccess | es_ES |
dc.subject | HIF1α | es_ES |
dc.subject | Glutamine | es_ES |
dc.subject | Aspartate biosynthesis | es_ES |
dc.subject | GOT1 | es_ES |
dc.subject | GOT2 | es_ES |
dc.subject | Cancer | es_ES |
dc.subject | Proliferation | es_ES |
dc.subject | Oxygen | es_ES |
dc.subject | Renal cell carcinoma | es_ES |
dc.title | HIF1α suppresses tumor cell proliferation through inhibition of aspartate biosynthesis | es_ES |
dc.type | artículo | es_ES |
dc.identifier.doi | 10.1016/j.celrep.2019.01.106 | - |
dc.description.peerreviewed | Peer reviewed | es_ES |
dc.relation.publisherversion | https://doi.org/10.1016/j.celrep.2019.01.106 | es_ES |
dc.identifier.e-issn | 2211-1247 | - |
dc.rights.license | https://creativecommons.org/licenses/by-nc-nd/4.0/ | es_ES |
dc.contributor.funder | Agencia Estatal de Investigación (España) | - |
dc.contributor.funder | Ministerio de Economía y Competitividad (España) | es_ES |
dc.contributor.funder | Comunidad de Madrid | es_ES |
dc.contributor.funder | Fundació La Marató de TV3 | es_ES |
dc.contributor.funder | European Commission | es_ES |
dc.contributor.funder | Research Foundation - Flanders | es_ES |
dc.contributor.funder | Universidad de Castilla La Mancha | es_ES |
dc.contributor.funder | Ministerio de Educación y Ciencia (España) | es_ES |
dc.contributor.funder | Ministerio de Ciencia, Innovación y Universidades (España) | es_ES |
dc.contributor.funder | Fundación Leticia Castillejo | es_ES |
dc.relation.csic | Sí | es_ES |
oprm.item.hasRevision | no ko 0 false | * |
dc.identifier.funder | http://dx.doi.org/10.13039/501100003329 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100000780 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100003130 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/100012818 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/100008666 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100007480 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100011033 | es_ES |
dc.identifier.pmid | 30811976 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | With Fulltext | - |
item.cerifentitytype | Publications | - |
item.openairetype | artículo | - |
item.languageiso639-1 | en | - |
item.grantfulltext | open | - |
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hifbio.pdf | 2,18 MB | Adobe PDF | Visualizar/Abrir |
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