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SM ISO690:2012 WALDT, 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 |
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Journal of Neuroscience Methods | |
Numărul 356 / 2021 / ISSN 0165-0270 /ISSNe 1872-678X | |
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DOI:https://doi.org/10.1016/j.jneumeth.2021.109141 | |
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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. |
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Cuvinte-cheie Crispr/Cas, Meningioma, Neurofibromatosis type 2 (NF2) |
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