PR-LncRNA signature regulates glioma cell activity through expression of SOX factors

Abstract Long non-coding RNAs (LncRNAs) have emerged as a relevant class of genome regulators involved in a broad range of biological processes and with important roles in tumor initiation and malignant progression. We have previously identified a p53-regulated tumor suppressor signature of LncRNAs...

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Autores principales:	Sergio Torres-Bayona, Paula Aldaz, Jaione Auzmendi-Iriarte, Ander Saenz-Antoñanzas, Idoia Garcia, Mariano Arrazola, Daniela Gerovska, Jose Undabeitia, Arrate Querejeta, Larraitz Egaña, Jorge Villanúa, Irune Ruiz, Cristina Sarasqueta, Enrique Urculo, Marcos J. Araúzo-Bravo, Maite Huarte, Nicolas Samprón, Ander Matheu
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c872a6ab60e84e74817e34215cc393e2
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spelling	oai:doaj.org-article:c872a6ab60e84e74817e34215cc393e22021-12-02T11:40:47ZPR-LncRNA signature regulates glioma cell activity through expression of SOX factors10.1038/s41598-018-30836-52045-2322https://doaj.org/article/c872a6ab60e84e74817e34215cc393e22018-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-30836-5https://doaj.org/toc/2045-2322Abstract Long non-coding RNAs (LncRNAs) have emerged as a relevant class of genome regulators involved in a broad range of biological processes and with important roles in tumor initiation and malignant progression. We have previously identified a p53-regulated tumor suppressor signature of LncRNAs (PR-LncRNAs) in colorectal cancer. Our aim was to identify the expression and function of this signature in gliomas. We found that the expression of the four PR-LncRNAs tested was high in human low-grade glioma samples and diminished with increasing grade of disease, being the lowest in glioblastoma samples. Functional assays demonstrated that PR-LncRNA silencing increased glioma cell proliferation and oncosphere formation. Mechanistically, we found an inverse correlation between PR-LncRNA expression and SOX1, SOX2 and SOX9 stem cell factors in human glioma biopsies and in glioma cells in vitro. Moreover, knock-down of SOX activity abolished the effect of PR-LncRNA silencing in glioma cell activity. In conclusion, our results demonstrate that the expression and function of PR-LncRNAs are significantly altered in gliomagenesis and that their activity is mediated by SOX factors. These results may provide important insights into the mechanisms responsible for glioblastoma pathogenesis.Sergio Torres-BayonaPaula AldazJaione Auzmendi-IriarteAnder Saenz-AntoñanzasIdoia GarciaMariano ArrazolaDaniela GerovskaJose UndabeitiaArrate QuerejetaLarraitz EgañaJorge VillanúaIrune RuizCristina SarasquetaEnrique UrculoMarcos J. Araúzo-BravoMaite HuarteNicolas SamprónAnder MatheuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-12 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sergio Torres-Bayona Paula Aldaz Jaione Auzmendi-Iriarte Ander Saenz-Antoñanzas Idoia Garcia Mariano Arrazola Daniela Gerovska Jose Undabeitia Arrate Querejeta Larraitz Egaña Jorge Villanúa Irune Ruiz Cristina Sarasqueta Enrique Urculo Marcos J. Araúzo-Bravo Maite Huarte Nicolas Samprón Ander Matheu PR-LncRNA signature regulates glioma cell activity through expression of SOX factors
description	Abstract Long non-coding RNAs (LncRNAs) have emerged as a relevant class of genome regulators involved in a broad range of biological processes and with important roles in tumor initiation and malignant progression. We have previously identified a p53-regulated tumor suppressor signature of LncRNAs (PR-LncRNAs) in colorectal cancer. Our aim was to identify the expression and function of this signature in gliomas. We found that the expression of the four PR-LncRNAs tested was high in human low-grade glioma samples and diminished with increasing grade of disease, being the lowest in glioblastoma samples. Functional assays demonstrated that PR-LncRNA silencing increased glioma cell proliferation and oncosphere formation. Mechanistically, we found an inverse correlation between PR-LncRNA expression and SOX1, SOX2 and SOX9 stem cell factors in human glioma biopsies and in glioma cells in vitro. Moreover, knock-down of SOX activity abolished the effect of PR-LncRNA silencing in glioma cell activity. In conclusion, our results demonstrate that the expression and function of PR-LncRNAs are significantly altered in gliomagenesis and that their activity is mediated by SOX factors. These results may provide important insights into the mechanisms responsible for glioblastoma pathogenesis.
format	article
author	Sergio Torres-Bayona Paula Aldaz Jaione Auzmendi-Iriarte Ander Saenz-Antoñanzas Idoia Garcia Mariano Arrazola Daniela Gerovska Jose Undabeitia Arrate Querejeta Larraitz Egaña Jorge Villanúa Irune Ruiz Cristina Sarasqueta Enrique Urculo Marcos J. Araúzo-Bravo Maite Huarte Nicolas Samprón Ander Matheu
author_facet	Sergio Torres-Bayona Paula Aldaz Jaione Auzmendi-Iriarte Ander Saenz-Antoñanzas Idoia Garcia Mariano Arrazola Daniela Gerovska Jose Undabeitia Arrate Querejeta Larraitz Egaña Jorge Villanúa Irune Ruiz Cristina Sarasqueta Enrique Urculo Marcos J. Araúzo-Bravo Maite Huarte Nicolas Samprón Ander Matheu
author_sort	Sergio Torres-Bayona
title	PR-LncRNA signature regulates glioma cell activity through expression of SOX factors
title_short	PR-LncRNA signature regulates glioma cell activity through expression of SOX factors
title_full	PR-LncRNA signature regulates glioma cell activity through expression of SOX factors
title_fullStr	PR-LncRNA signature regulates glioma cell activity through expression of SOX factors
title_full_unstemmed	PR-LncRNA signature regulates glioma cell activity through expression of SOX factors
title_sort	pr-lncrna signature regulates glioma cell activity through expression of sox factors
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/c872a6ab60e84e74817e34215cc393e2
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PR-LncRNA signature regulates glioma cell activity through expression of SOX factors

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