Modeling NF2 with human arachnoidal and meningioma cell culture systems: NF2 silencing reflects the benign character of tumor growth

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Modeling NF2 with human arachnoidal and meningioma cell culture systems: NF2 silencing reflects the benign character of tumor growth

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Title: Modeling NF2 with human arachnoidal and meningioma cell culture systems: NF2 silencing reflects the benign character of tumor growth
Author: James, Marianne; Lelke, Johanna M.; MacCollin, Mia; Plotkin, Scott Randall; Stemmer-Rachamimov, Anat; Ramesh, Vijaya; Gusella, James Francis

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Citation: James, Marianne F., Johanna M. Lelke, Mia MacCollin, Scott R. Plotkin, Anat O. Stemmer-Rachamimov, Vijaya Ramesh, and James F. Gusella. 2008. “Modeling NF2 with Human Arachnoidal and Meningioma Cell Culture Systems: NF2 Silencing Reflects the Benign Character of Tumor Growth.” Neurobiology of Disease 29 (2) (February): 278–292. doi:10.1016/j.nbd.2007.09.002.
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Abstract: Meningiomas, common tumors arising from arachnoidal cells of the meninges, may occur sporadically, or in association with the inherited disorder, neurofibromatosis 2 (NF2). Most sporadic meningiomas result from NF2 inactivation, resulting in loss of tumor suppressor merlin, implicated in regulating membrane-cytoskeletal organization. To investigate merlin function in an authentic target cell type for NF2 tumor formation, we established primary cultures from genetically-matched meningioma and normal arachnoidal tissues. Our studies revealed novel and distinct cell biological and biochemical properties unique to merlin-deficient meningioma cells compared to merlin-expressing arachnoidal and meningioma cells, and other NF2-deficient cell types. Merlin-deficient meningioma cells displayed cytoskeletal and cell contact defects, altered cell morphology and growth properties, most notably cell senescence, implicating the activation of senescence pathways in limiting benign meningioma growth. Merlin suppression by RNAi in arachnoidal cells replicated merlin-deficient meningioma features, thus establishing these cell systems as disease-relevant models for studying NF2 tumorigenesis.
Published Version: 10.1016/j.nbd.2007.09.002
Other Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2266821/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:32631238
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