Blockade of the SNARE Protein Syntaxin 1 Inhibits Glioblastoma Tumor Growth
Glioblastoma (GBM) is the most prevalent adult brain tumor, with virtually no cure, and with a median overall survival of 15 months from diagnosis despite of the treatment. SNARE proteins mediate membrane fusion events in cells and are essential for many cellular processes including exocytosis and n...
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Published in | PloS one Vol. 10; no. 3; p. e0119707 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Public Library of Science
24.03.2015
Public Library of Science (PLoS) |
Subjects | |
Online Access | Get full text |
ISSN | 1932-6203 1932-6203 |
DOI | 10.1371/journal.pone.0119707 |
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Abstract | Glioblastoma (GBM) is the most prevalent adult brain tumor, with virtually no cure, and with a median overall survival of 15 months from diagnosis despite of the treatment. SNARE proteins mediate membrane fusion events in cells and are essential for many cellular processes including exocytosis and neurotransmission, intracellular trafficking and cell migration. Here we show that the blockade of the SNARE protein Syntaxin 1 (Stx1) function impairs GBM cell proliferation. We show that Stx1 loss-of-function in GBM cells, through ShRNA lentiviral transduction, a Stx1 dominant negative and botulinum toxins, dramatically reduces the growth of GBM after grafting U373 cells into the brain of immune compromised mice. Interestingly, Stx1 role on GBM progression may not be restricted just to cell proliferation since the blockade of Stx1 also reduces in vitro GBM cell invasiveness suggesting a role in several processes relevant for tumor progression. Altogether, our findings indicate that the blockade of SNARE proteins may represent a novel therapeutic tool against GBM. |
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AbstractList | Glioblastoma (GBM) is the most prevalent adult brain tumor, with virtually no cure, and with a median overall survival of 15 months from diagnosis despite of the treatment. SNARE proteins mediate membrane fusion events in cells and are essential for many cellular processes including exocytosis and neurotransmission, intracellular trafficking and cell migration. Here we show that the blockade of the SNARE protein Syntaxin 1 (Stx1) function impairs GBM cell proliferation. We show that Stx1 loss-of-function in GBM cells, through ShRNA lentiviral transduction, a Stx1 dominant negative and botulinum toxins, dramatically reduces the growth of GBM after grafting U373 cells into the brain of immune compromised mice. Interestingly, Stx1 role on GBM progression may not be restricted just to cell proliferation since the blockade of Stx1 also reduces in vitro GBM cell invasiveness suggesting a role in several processes relevant for tumor progression. Altogether, our findings indicate that the blockade of SNARE proteins may represent a novel therapeutic tool against GBM. Glioblastoma (GBM) is the most prevalent adult brain tumor, with virtually no cure, and with a median overall survival of 15 months from diagnosis despite of the treatment. SNARE pro- teins mediate membrane fusion events in cells and are essential for many cellular process- es including exocytosis and neurotransmission, intracellular trafficking and cell migration. Here we show that the blockade of the SNARE protein Syntaxin 1 (Stx1) function impairs GBM cell proliferation. We show that Stx1 loss-of-function in GBM cells, through ShRNA lentiviral transduction, a Stx1 dominant negative and botulinum toxins, dramatically reduces the growth of GBM after grafting U373 cells into the brain of immune compromised mice. In- terestingly, Stx1 role on GBM progression may not be restricted just to cell proliferation since the blockade of Stx1 also reduces in vitro GBM cell invasiveness suggesting a role in several processes relevant for tumor progression. Altogether, our findings indicate that the blockade of SNARE proteins may represent a novel therapeutic tool against GBM. Glioblastoma (GBM) is the most prevalent adult brain tumor, with virtually no cure, and with a median overall survival of 15 months from diagnosis despite of the treatment. SNARE proteins mediate membrane fusion events in cells and are essential for many cellular processes including exocytosis and neurotransmission, intracellular trafficking and cell migration. Here we show that the blockade of the SNARE protein Syntaxin 1 (Stx1) function impairs GBM cell proliferation. We show that Stx1 loss-of-function in GBM cells, through ShRNA lentiviral transduction, a Stx1 dominant negative and botulinum toxins, dramatically reduces the growth of GBM after grafting U373 cells into the brain of immune compromised mice. Interestingly, Stx1 role on GBM progression may not be restricted just to cell proliferation since the blockade of Stx1 also reduces in vitro GBM cell invasiveness suggesting a role in several processes relevant for tumor progression. Altogether, our findings indicate that the blockade of SNARE proteins may represent a novel therapeutic tool against GBM.Glioblastoma (GBM) is the most prevalent adult brain tumor, with virtually no cure, and with a median overall survival of 15 months from diagnosis despite of the treatment. SNARE proteins mediate membrane fusion events in cells and are essential for many cellular processes including exocytosis and neurotransmission, intracellular trafficking and cell migration. Here we show that the blockade of the SNARE protein Syntaxin 1 (Stx1) function impairs GBM cell proliferation. We show that Stx1 loss-of-function in GBM cells, through ShRNA lentiviral transduction, a Stx1 dominant negative and botulinum toxins, dramatically reduces the growth of GBM after grafting U373 cells into the brain of immune compromised mice. Interestingly, Stx1 role on GBM progression may not be restricted just to cell proliferation since the blockade of Stx1 also reduces in vitro GBM cell invasiveness suggesting a role in several processes relevant for tumor progression. Altogether, our findings indicate that the blockade of SNARE proteins may represent a novel therapeutic tool against GBM. |
Audience | Academic |
Author | Cotrufo, Tiziana Barrecheguren, Pablo José Martínez-Mármol, Ramón Pazos, Irene Seoane, Joan Soriano, Eduardo Gonzàlez-Juncà, Alba Meffre, Delphine Olivé, Núria Ulloa, Fausto |
AuthorAffiliation | 3 Translational Research Program, Vall d'Hebron Institute of Oncology (VHIO), Vall d’Hebron University Hospital, 08035, Barcelona, Spain 5 Institute for Research in Biomedicine (IRB), Cell and Developmental Biology Program, Barcelona, 08028, Spain 6 Vall d´Hebron Institute of Research (VHIR), 08035, Barcelona, Spain 1 Department of Cell Biology, University of Barcelona, Parc Cientific de Barcelona, 08028, Barcelona, Spain 2 Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), ISCIII, 28031, Madrid, Spain Swedish Neuroscience Institute, UNITED STATES 4 Universitat Autònoma de Barcelona, 08193, Cerdanyola del Vallès, Spain 7 Institució Catalana de Recerca i Estudis Avançats (ICREA), 08010, Barcelona, Spain |
AuthorAffiliation_xml | – name: 3 Translational Research Program, Vall d'Hebron Institute of Oncology (VHIO), Vall d’Hebron University Hospital, 08035, Barcelona, Spain – name: 4 Universitat Autònoma de Barcelona, 08193, Cerdanyola del Vallès, Spain – name: Swedish Neuroscience Institute, UNITED STATES – name: 1 Department of Cell Biology, University of Barcelona, Parc Cientific de Barcelona, 08028, Barcelona, Spain – name: 6 Vall d´Hebron Institute of Research (VHIR), 08035, Barcelona, Spain – name: 7 Institució Catalana de Recerca i Estudis Avançats (ICREA), 08010, Barcelona, Spain – name: 2 Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), ISCIII, 28031, Madrid, Spain – name: 5 Institute for Research in Biomedicine (IRB), Cell and Developmental Biology Program, Barcelona, 08028, Spain |
Author_xml | – sequence: 1 givenname: Fausto surname: Ulloa fullname: Ulloa, Fausto – sequence: 2 givenname: Alba surname: Gonzàlez-Juncà fullname: Gonzàlez-Juncà, Alba – sequence: 3 givenname: Delphine surname: Meffre fullname: Meffre, Delphine – sequence: 4 givenname: Pablo José surname: Barrecheguren fullname: Barrecheguren, Pablo José – sequence: 5 givenname: Ramón surname: Martínez-Mármol fullname: Martínez-Mármol, Ramón – sequence: 6 givenname: Irene surname: Pazos fullname: Pazos, Irene – sequence: 7 givenname: Núria surname: Olivé fullname: Olivé, Núria – sequence: 8 givenname: Tiziana surname: Cotrufo fullname: Cotrufo, Tiziana – sequence: 9 givenname: Joan surname: Seoane fullname: Seoane, Joan – sequence: 10 givenname: Eduardo surname: Soriano fullname: Soriano, Eduardo |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: ES JS FU. Performed the experiments: FU AG DM PB RM IP NO TC. Analyzed the data: FU AG DM PB RM IP NO TC JS ES. Contributed reagents/materials/analysis tools: FU AG DM PB RM IP NO TC JS ES. Wrote the paper: ES JS FU. |
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SubjectTerms | Animals Biology Blotting, Western Botulinum toxin Botulinum Toxins - pharmacology Brain Brain cancer Brain research Brain tumors Bromodeoxyuridine Cancer treatment Cell Line, Tumor Cell migration Cell proliferation Cell Proliferation - drug effects Cognitive science Cytoskeletal proteins Exocytosis Flow Cytometry Glioblastoma Glioblastoma - drug therapy Glioblastoma - physiopathology Glioblastomas Glioma Gliomas Growth Humans Invasiveness Lentivirus Membrane fusion Mice Neoplasm Invasiveness - prevention & control Nervous system Neuroscience Neurotransmission Proteins Proteïnes citosquelètiques RNA, Small Interfering - genetics RNA, Small Interfering - pharmacology SNAP receptors Statistics, Nonparametric Syntaxin Syntaxin 1 Syntaxin 1 - antagonists & inhibitors Toxins Transduction, Genetic - methods Tumors |
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