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dc.contributor.authorMorales Hernández, Antonio-
dc.contributor.authorGonzález Rico, Francisco Javier-
dc.contributor.authorRomán García, Ángel Carlos-
dc.contributor.authorRico Leo, Eva María-
dc.contributor.authorÁlvarez Barrientos, Alberto-
dc.contributor.authorSánchez Ruiz, Laura-
dc.contributor.authorMacia Ortega, Ángela-
dc.contributor.authorRodríguez Heras, Sara-
dc.contributor.authorGarcía Pérez, José Luis-
dc.contributor.authorMerino Fernández, Jaime María-
dc.contributor.authorFernández Salguero, Pedro María-
dc.description.abstractCell differentiation is a central process in development and in cancer growth and dissemination. OCT4 (POU5F1) and NANOG are essential for cell stemness and pluripotency; yet, the mechanisms that regulate their expression remain largely unknown. Repetitive elements account for almost half of the Human Genome; still, their role in gene regulation is poorly understood. Here, we show that the dioxin receptor (AHR) leads to differentiation of human carcinoma cells through the transcriptional upregulation of Alu retrotransposons, whose RNA transcripts can repress pluripotency genes. Despite the genome-wide presence of Alu elements, we provide evidences that those located at the NANOG and OCT4 promoters bind AHR, are transcribed by RNA polymerase-III and repress NANOG and OCT4 in differentiated cells. OCT4 and NANOG repression likely involves processing of Alu-derived transcripts through the miRNA machinery involving the Microprocessor and RISC. Consistently, stable AHR knockdown led to basal undifferentiation, impaired Alus transcription and blockade of OCT4 and NANOG repression. We suggest that transcripts produced from AHR-regulated Alu retrotransposons may control the expression of stemness genes OCT4 and NANOG during differentiation of carcinoma cells. The control of discrete Alu elements by specific transcription factors may have a dynamic role in genome regulation under physiological and diseased conditions.es_ES
dc.description.sponsorshipTrabajo financiado por: Ministerio de Economía y Competitividad. Proyectos BFU2011-22678, SAF2014-51813-R (I+D+i) para Pedro María Fernández Salguero Ministerio de Economía y Competitividad, Instituto Carlos III, Red Temática de Investigación Cooperativa en Cáncer Junta de Extremadura. Ayudas GR10008, GR15008 CICE-FEDER-P09-CTS-4980, CICE-FEDERP12-CTS-2256, Plan Nacional de I+D+I 2008–2011 y 2013–2016 (FIS-FEDER-PI11/01489, FIS-FEDERPI14/02152), PCIN-2014-115-ERA-NET NEURON II, para José Luis García Pérez European Research Council ERC-Consolidator ERC-STG-2012-233764 International Early Career Scientist Beca de la Howard Hughes Medical Institute IECS-55007420 Programa Unión Europea de Fondos FEDERes_ES
dc.format.extent19 p.es_ES
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 España*
dc.subjectDiferenciación celulares_ES
dc.subjectRegulación de geneses_ES
dc.subjectCélulas de carcinomaes_ES
dc.subjectElementos discretos de Alues_ES
dc.subjectCell differentiationes_ES
dc.subjectGene regulationes_ES
dc.subjectCarcinoma cellses_ES
dc.subjectDiscrete Alu elementses_ES
dc.titleAlu retrotransposons promote differentiation of human carcinoma cells through the aryl hydrocarbon receptores_ES
dc.subject.unesco2407 Biología Celulares_ES
europeana.dataProviderUniversidad de Extremadura. Españaes_ES
dc.identifier.bibliographicCitationMorales Hernández, A.; González Rico, F. J.; Román García, A. C.; Rico Leo, E.M.; Álvarez Barrientos, A.; Sánchez Ruiz, L. y Macia Ortega, A. [et al.]. (2016). Alu retrotransposons promote differentiation of human carcinoma cells through the aryl hydrocarbon receptor. Nucleid acids research, 44, 10. 4665-4683. ESSN 1362-4962es_ES
dc.contributor.affiliationCSIC-Instituto Cajal. Madrides_ES
dc.contributor.affiliationUniversidad de Extremadura. Departamento de Bioquímica, Biología Molecular y Genéticaes_ES
dc.contributor.affiliationUniversidad de Granada-
dc.identifier.publicationtitleNucleid acids researches_ES
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