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Radiation Increases Functional KCa3.1 Expression and Invasiveness in Glioblastoma
Glioblastoma (GBM) is a deadly brain tumor, with fast recurrence even after surgical intervention, radio- and chemotherapies. One of the reasons for relapse is the early invasion of surrounding brain parenchyma by GBM, rendering tumor eradication difficult. Recent studies demonstrate that, in additi...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468446/ https://www.ncbi.nlm.nih.gov/pubmed/30813636 http://dx.doi.org/10.3390/cancers11030279 |
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author | D’Alessandro, Giuseppina Monaco, Lucia Catacuzzeno, Luigi Antonangeli, Fabrizio Santoro, Antonio Esposito, Vincenzo Franciolini, Fabio Wulff, Heike Limatola, Cristina |
author_facet | D’Alessandro, Giuseppina Monaco, Lucia Catacuzzeno, Luigi Antonangeli, Fabrizio Santoro, Antonio Esposito, Vincenzo Franciolini, Fabio Wulff, Heike Limatola, Cristina |
author_sort | D’Alessandro, Giuseppina |
collection | PubMed |
description | Glioblastoma (GBM) is a deadly brain tumor, with fast recurrence even after surgical intervention, radio- and chemotherapies. One of the reasons for relapse is the early invasion of surrounding brain parenchyma by GBM, rendering tumor eradication difficult. Recent studies demonstrate that, in addition to eliminate possible residual tumoral cells after surgery, radiation stimulates the infiltrative behavior of GBM cells. The intermediate conductance of Ca(2+)-activated potassium channels (KCa3.1) play an important role in regulating the migration of GBM. Here, we show that high dose radiation of patient-derived GBM cells increases their invasion, and induces the transcription of key genes related to these functions, including the IL-4/IL-4R pair. In addition, we demonstrate that radiation increases the expression of KCa3.1 channels, and that their pharmacological inhibition counteracts the pro-invasive phenotype induced by radiation in tumor cells. Our data describe a possible approach to treat tumor resistance that follows radiation therapy in GBM patients. |
format | Online Article Text |
id | pubmed-6468446 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-64684462019-04-24 Radiation Increases Functional KCa3.1 Expression and Invasiveness in Glioblastoma D’Alessandro, Giuseppina Monaco, Lucia Catacuzzeno, Luigi Antonangeli, Fabrizio Santoro, Antonio Esposito, Vincenzo Franciolini, Fabio Wulff, Heike Limatola, Cristina Cancers (Basel) Article Glioblastoma (GBM) is a deadly brain tumor, with fast recurrence even after surgical intervention, radio- and chemotherapies. One of the reasons for relapse is the early invasion of surrounding brain parenchyma by GBM, rendering tumor eradication difficult. Recent studies demonstrate that, in addition to eliminate possible residual tumoral cells after surgery, radiation stimulates the infiltrative behavior of GBM cells. The intermediate conductance of Ca(2+)-activated potassium channels (KCa3.1) play an important role in regulating the migration of GBM. Here, we show that high dose radiation of patient-derived GBM cells increases their invasion, and induces the transcription of key genes related to these functions, including the IL-4/IL-4R pair. In addition, we demonstrate that radiation increases the expression of KCa3.1 channels, and that their pharmacological inhibition counteracts the pro-invasive phenotype induced by radiation in tumor cells. Our data describe a possible approach to treat tumor resistance that follows radiation therapy in GBM patients. MDPI 2019-02-26 /pmc/articles/PMC6468446/ /pubmed/30813636 http://dx.doi.org/10.3390/cancers11030279 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article D’Alessandro, Giuseppina Monaco, Lucia Catacuzzeno, Luigi Antonangeli, Fabrizio Santoro, Antonio Esposito, Vincenzo Franciolini, Fabio Wulff, Heike Limatola, Cristina Radiation Increases Functional KCa3.1 Expression and Invasiveness in Glioblastoma |
title | Radiation Increases Functional KCa3.1 Expression and Invasiveness in Glioblastoma |
title_full | Radiation Increases Functional KCa3.1 Expression and Invasiveness in Glioblastoma |
title_fullStr | Radiation Increases Functional KCa3.1 Expression and Invasiveness in Glioblastoma |
title_full_unstemmed | Radiation Increases Functional KCa3.1 Expression and Invasiveness in Glioblastoma |
title_short | Radiation Increases Functional KCa3.1 Expression and Invasiveness in Glioblastoma |
title_sort | radiation increases functional kca3.1 expression and invasiveness in glioblastoma |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468446/ https://www.ncbi.nlm.nih.gov/pubmed/30813636 http://dx.doi.org/10.3390/cancers11030279 |
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