Abstract
One common genetic change in anaplastic meningiomas is amplification of chromosome 17q23 containing the S6 kinase (S6K) gene. We show, for the first time to our knowledge, increased S6K mRNA expression in anaplastic meningiomas compared with benign tumors. To evaluate S6K as a candidate meningioma progression gene, we generated IOMM-Lee human meningioma cell lines overexpressing S6K. Whereas no effect of S6K overexpression on meningioma cell growth, motility, or adhesion was observed in vitro, S6K overexpression resulted in increased tumor size in vivo. Collectively, these results suggest that S6K is functionally important for meningioma progression and may represent a target for future meningioma therapy.
Copyright 2004 American Neurological Association
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Blotting, Western / methods
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Cell Count
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Cell Division / physiology
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Cell Line, Tumor
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Cell Movement / physiology
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Disease Progression
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Gene Expression Regulation*
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Humans
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Meningeal Neoplasms / genetics
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Meningeal Neoplasms / metabolism*
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Meningeal Neoplasms / pathology
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Meningioma / genetics
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Meningioma / metabolism*
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Meningioma / pathology
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Mice
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Mice, Nude
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RNA, Messenger / metabolism
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Reverse Transcriptase Polymerase Chain Reaction / methods
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Ribosomal Protein S6 Kinases / genetics
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Ribosomal Protein S6 Kinases / metabolism*
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Ribosomal Protein S6 Kinases / physiology
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Time Factors
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Transfection / methods
Substances
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RNA, Messenger
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Ribosomal Protein S6 Kinases