| Conţinutul numărului revistei |
| Articolul precedent |
| Articolul urmator |
 293 0 |
 SM ISO690:2012WALDT, Natalie, KESSELER, Christoph, FALA, Paula, JOHN, Peter, KIRCHES, Elmar J.F., ANGENSTEIN , Frank, MAWRIN, Christian. Crispr/Cas-based modeling of NF2 loss in meningioma cells. In: Journal of Neuroscience Methods , 2021, nr. 356, p. 0. ISSN 0165-0270. DOI: https://doi.org/10.1016/j.jneumeth.2021.109141 |
| EXPORT metadate: Google Scholar Crossref CERIF DataCite Dublin Core |
| Journal of Neuroscience Methods | |
| Numărul 356 / 2021 / ISSN 0165-0270 /ISSNe 1872-678X | |
|
|
| DOI:https://doi.org/10.1016/j.jneumeth.2021.109141 | |
| Pag. 0-0 | |
| Rezumat | |
Background: Alterations of the neurofibromatosis type 2 gene (NF2) occur in more than fifty percent of sporadic meningiomas. Meningiomas develop frequently in the setting of the hereditary tumor syndrome NF2. Investigation of potential drug-based treatment options has been limited by the lack of appropriate in vitro and in vivo models. New methods: Using Crispr/Cas gene editing, of the malignant meningioma cell line IOMM-Lee, we generated a pair of cell clones characterized by either stable knockout of NF2 and loss of the protein product merlin or retained merlin protein (transfected control without gRNA). Results: IOMM-Lee cells lacking NF2 showed reduced apoptosis and formed bigger colonies compared to control IOMM-Lee cells. Treatment of non-transfected IOMM-Lee cells with the focal adhesion kinase (FAK) inhibitor GSK2256098 resulted in reduced colony sizes. Orthotopic mouse xenografts showed the formation of convexity tumors typical for meningiomas with NF2-depleted and control cells. Comparison with existing methods: No orthotopic meningioma models with genetically-engineered cell pairs are available so far. Conclusion: Our model based on Crispr/Cas-based gene editing provides paired meningioma cells suitable to study functional consequences and therapeutic accessibility of NF2/merlin loss. |
|
| Cuvinte-cheie Crispr/Cas, Meningioma, Neurofibromatosis type 2 (NF2) |
|
|
Dublin Core Export
<?xml version='1.0' encoding='utf-8'?> <oai_dc:dc xmlns:dc='http://purl.org/dc/elements/1.1/' xmlns:oai_dc='http://www.openarchives.org/OAI/2.0/oai_dc/' xmlns:xsi='http://www.w3.org/2001/XMLSchema-instance' xsi:schemaLocation='http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd'> <dc:creator>Waldt, N.</dc:creator> <dc:creator>Kesseler, C.</dc:creator> <dc:creator>Fala, P.</dc:creator> <dc:creator>John, P.</dc:creator> <dc:creator>Kirches, E.</dc:creator> <dc:creator>Angenstein , F.</dc:creator> <dc:creator>Mawrin, C.</dc:creator> <dc:date>2021-05-15</dc:date> <dc:description xml:lang='en'><p>Background: Alterations of the neurofibromatosis type 2 gene (NF2) occur in more than fifty percent of sporadic meningiomas. Meningiomas develop frequently in the setting of the hereditary tumor syndrome NF2. Investigation of potential drug-based treatment options has been limited by the lack of appropriate in vitro and in vivo models. New methods: Using Crispr/Cas gene editing, of the malignant meningioma cell line IOMM-Lee, we generated a pair of cell clones characterized by either stable knockout of NF2 and loss of the protein product merlin or retained merlin protein (transfected control without gRNA). Results: IOMM-Lee cells lacking NF2 showed reduced apoptosis and formed bigger colonies compared to control IOMM-Lee cells. Treatment of non-transfected IOMM-Lee cells with the focal adhesion kinase (FAK) inhibitor GSK2256098 resulted in reduced colony sizes. Orthotopic mouse xenografts showed the formation of convexity tumors typical for meningiomas with NF2-depleted and control cells. Comparison with existing methods: No orthotopic meningioma models with genetically-engineered cell pairs are available so far. Conclusion: Our model based on Crispr/Cas-based gene editing provides paired meningioma cells suitable to study functional consequences and therapeutic accessibility of NF2/merlin loss. </p></dc:description> <dc:identifier>10.1016/j.jneumeth.2021.109141</dc:identifier> <dc:source>Journal of Neuroscience Methods (356) 0-0</dc:source> <dc:subject>Crispr/Cas</dc:subject> <dc:subject>Meningioma</dc:subject> <dc:subject>Neurofibromatosis type 2 (NF2)</dc:subject> <dc:title>Crispr/Cas-based modeling of NF2 loss in meningioma cells</dc:title> <dc:type>info:eu-repo/semantics/article</dc:type> </oai_dc:dc>
|
|
|
