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Role of Btg2 in the Progression of a PDGF-Induced Oligodendroglioma Model
Tumor progression is a key aspect in oncology. Not even the overexpression of a powerful oncogenic stimulus such as platelet derived growth factor-B (PDGF-B) is sufficient per se to confer full malignancy to cells. In previous studies we showed that neural progenitors overexpressing PDGF-B need to u...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Molecular Diversity Preservation International (MDPI)
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509603/ https://www.ncbi.nlm.nih.gov/pubmed/23203087 http://dx.doi.org/10.3390/ijms131114667 |
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author | Appolloni, Irene Curreli, Sebastiano Caviglia, Sara Barilari, Manuela Gambini, Eleonora Pagano, Aldo Malatesta, Paolo |
author_facet | Appolloni, Irene Curreli, Sebastiano Caviglia, Sara Barilari, Manuela Gambini, Eleonora Pagano, Aldo Malatesta, Paolo |
author_sort | Appolloni, Irene |
collection | PubMed |
description | Tumor progression is a key aspect in oncology. Not even the overexpression of a powerful oncogenic stimulus such as platelet derived growth factor-B (PDGF-B) is sufficient per se to confer full malignancy to cells. In previous studies we showed that neural progenitors overexpressing PDGF-B need to undergo progression to acquire the capability to give rise to secondary tumor following transplant. By comparing the expression profile of PDGF-expressing cells before and after progression, we found that progressed tumors consistently downregulate the expression of the antiproliferative gene Btg2. We therefore tested whether the downregulation of Btg2 is sufficient and necessary for glioma progression with loss and gain of function experiments. Our results show that downregulation of Btg2 is not sufficient but is necessary for tumor progression since the re-introduction of Btg2 in fully progressed tumors dramatically impairs their gliomagenic potential. These results suggest an important role of Btg2 in glioma progression. Accordingly with this view, the analysis of public datasets of human gliomas showed that reduced level of Btg2 expression correlates with a significantly worse prognosis. |
format | Online Article Text |
id | pubmed-3509603 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Molecular Diversity Preservation International (MDPI) |
record_format | MEDLINE/PubMed |
spelling | pubmed-35096032013-01-09 Role of Btg2 in the Progression of a PDGF-Induced Oligodendroglioma Model Appolloni, Irene Curreli, Sebastiano Caviglia, Sara Barilari, Manuela Gambini, Eleonora Pagano, Aldo Malatesta, Paolo Int J Mol Sci Article Tumor progression is a key aspect in oncology. Not even the overexpression of a powerful oncogenic stimulus such as platelet derived growth factor-B (PDGF-B) is sufficient per se to confer full malignancy to cells. In previous studies we showed that neural progenitors overexpressing PDGF-B need to undergo progression to acquire the capability to give rise to secondary tumor following transplant. By comparing the expression profile of PDGF-expressing cells before and after progression, we found that progressed tumors consistently downregulate the expression of the antiproliferative gene Btg2. We therefore tested whether the downregulation of Btg2 is sufficient and necessary for glioma progression with loss and gain of function experiments. Our results show that downregulation of Btg2 is not sufficient but is necessary for tumor progression since the re-introduction of Btg2 in fully progressed tumors dramatically impairs their gliomagenic potential. These results suggest an important role of Btg2 in glioma progression. Accordingly with this view, the analysis of public datasets of human gliomas showed that reduced level of Btg2 expression correlates with a significantly worse prognosis. Molecular Diversity Preservation International (MDPI) 2012-11-12 /pmc/articles/PMC3509603/ /pubmed/23203087 http://dx.doi.org/10.3390/ijms131114667 Text en © 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0). |
spellingShingle | Article Appolloni, Irene Curreli, Sebastiano Caviglia, Sara Barilari, Manuela Gambini, Eleonora Pagano, Aldo Malatesta, Paolo Role of Btg2 in the Progression of a PDGF-Induced Oligodendroglioma Model |
title | Role of Btg2 in the Progression of a PDGF-Induced Oligodendroglioma Model |
title_full | Role of Btg2 in the Progression of a PDGF-Induced Oligodendroglioma Model |
title_fullStr | Role of Btg2 in the Progression of a PDGF-Induced Oligodendroglioma Model |
title_full_unstemmed | Role of Btg2 in the Progression of a PDGF-Induced Oligodendroglioma Model |
title_short | Role of Btg2 in the Progression of a PDGF-Induced Oligodendroglioma Model |
title_sort | role of btg2 in the progression of a pdgf-induced oligodendroglioma model |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509603/ https://www.ncbi.nlm.nih.gov/pubmed/23203087 http://dx.doi.org/10.3390/ijms131114667 |
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