The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.

In the present study we evaluated the expression of the intermediate conductance calcium-activated potassium (KCa3.1) channel in human glioblastoma stem-like cells (CSCs) and investigated its role in cell motility. While the KCa3.1 channel is not expressed in neuronal- and glial-derived tissues of h...

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Autores principales:	Paola Ruggieri, Giorgio Mangino, Bernard Fioretti, Luigi Catacuzzeno, Rosa Puca, Donatella Ponti, Massimo Miscusi, Fabio Franciolini, Giuseppe Ragona, Antonella Calogero
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7903ea439cd84abfa306962aa0157d5b
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spelling	oai:doaj.org-article:7903ea439cd84abfa306962aa0157d5b2021-11-18T08:11:25ZThe inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.1932-620310.1371/journal.pone.0047825https://doaj.org/article/7903ea439cd84abfa306962aa0157d5b2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23110108/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203In the present study we evaluated the expression of the intermediate conductance calcium-activated potassium (KCa3.1) channel in human glioblastoma stem-like cells (CSCs) and investigated its role in cell motility. While the KCa3.1 channel is not expressed in neuronal- and glial-derived tissues of healthy individuals, both the KCa3.1 mRNA and protein are present in the glioblastoma tumor population, and are significantly enhanced in CSCs derived from both established cell line U87MG and a primary cell line, FCN9. Consistent with these data, voltage-independent and TRAM-34 sensitive potassium currents imputable to the KCa3.1 channel were recorded in the murine GL261 cell line and several primary human glioblastoma cells lines. Moreover, a significantly higher KCa3.1 current was recorded in U87MG-CD133 positive cells as compared to the U87MG-CD133 negative subpopulation. Further, we found that the tumor cell motility is strongly associated with KCa3.1 channel expression. Blockade of the KCa3.1 channel with the specific inhibitor TRAM-34 has in fact a greater impact on the motility of CSCs (reduction of 75%), which express a high level of KCa3.1 channel, than on the FCN9 parental population (reduction of 32%), where the KCa3.1 channel is expressed at lower level. Similar results were also observed with the CSCs derived from U87MG. Because invasion of surrounding tissues is one of the main causes of treatment failure in glioblastoma, these findings can be relevant for future development of novel cancer therapeutic drugs.Paola RuggieriGiorgio ManginoBernard FiorettiLuigi CatacuzzenoRosa PucaDonatella PontiMassimo MiscusiFabio FrancioliniGiuseppe RagonaAntonella CalogeroPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 10, p e47825 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Paola Ruggieri Giorgio Mangino Bernard Fioretti Luigi Catacuzzeno Rosa Puca Donatella Ponti Massimo Miscusi Fabio Franciolini Giuseppe Ragona Antonella Calogero The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.
description	In the present study we evaluated the expression of the intermediate conductance calcium-activated potassium (KCa3.1) channel in human glioblastoma stem-like cells (CSCs) and investigated its role in cell motility. While the KCa3.1 channel is not expressed in neuronal- and glial-derived tissues of healthy individuals, both the KCa3.1 mRNA and protein are present in the glioblastoma tumor population, and are significantly enhanced in CSCs derived from both established cell line U87MG and a primary cell line, FCN9. Consistent with these data, voltage-independent and TRAM-34 sensitive potassium currents imputable to the KCa3.1 channel were recorded in the murine GL261 cell line and several primary human glioblastoma cells lines. Moreover, a significantly higher KCa3.1 current was recorded in U87MG-CD133 positive cells as compared to the U87MG-CD133 negative subpopulation. Further, we found that the tumor cell motility is strongly associated with KCa3.1 channel expression. Blockade of the KCa3.1 channel with the specific inhibitor TRAM-34 has in fact a greater impact on the motility of CSCs (reduction of 75%), which express a high level of KCa3.1 channel, than on the FCN9 parental population (reduction of 32%), where the KCa3.1 channel is expressed at lower level. Similar results were also observed with the CSCs derived from U87MG. Because invasion of surrounding tissues is one of the main causes of treatment failure in glioblastoma, these findings can be relevant for future development of novel cancer therapeutic drugs.
format	article
author	Paola Ruggieri Giorgio Mangino Bernard Fioretti Luigi Catacuzzeno Rosa Puca Donatella Ponti Massimo Miscusi Fabio Franciolini Giuseppe Ragona Antonella Calogero
author_facet	Paola Ruggieri Giorgio Mangino Bernard Fioretti Luigi Catacuzzeno Rosa Puca Donatella Ponti Massimo Miscusi Fabio Franciolini Giuseppe Ragona Antonella Calogero
author_sort	Paola Ruggieri
title	The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.
title_short	The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.
title_full	The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.
title_fullStr	The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.
title_full_unstemmed	The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.
title_sort	inhibition of kca3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/7903ea439cd84abfa306962aa0157d5b
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The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.

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