Abstract
Several growth factors and their receptors are expressed in inappropriately high abundance in gliomas and are further upregulated during the transition from low- to high-grade malignancy. In glioma cells growth factors induce expression of mitogen-activated protein kinase (MAPK) pathways. Here we report that neomycin restrained glioma cell proliferation in vitro by inhibition of p42/44 MAPK and the cyclic AMP element binding protein (CREB)-directed transcription pathways. Since alteration of gene transcription by inhibition of specific transcriptional regulatory proteins has important therapeutic potential, neomycin offers great promise for treating cancer and other diseases associated with a sustained MAPK activity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Division / drug effects
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Cyclic AMP Response Element-Binding Protein / antagonists & inhibitors
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Cyclic AMP Response Element-Binding Protein / drug effects*
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Cyclic AMP Response Element-Binding Protein / metabolism
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Glioma / metabolism
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Immunohistochemistry
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Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors
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Mitogen-Activated Protein Kinase 1 / drug effects
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Mitogen-Activated Protein Kinase 1 / metabolism
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Mitogen-Activated Protein Kinase 3
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Mitogen-Activated Protein Kinases / antagonists & inhibitors
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Mitogen-Activated Protein Kinases / drug effects*
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Mitogen-Activated Protein Kinases / metabolism
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Neomycin / pharmacology*
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Protein Synthesis Inhibitors / pharmacokinetics*
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Rats
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Tumor Cells, Cultured
Substances
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Cyclic AMP Response Element-Binding Protein
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Protein Synthesis Inhibitors
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Mitogen-Activated Protein Kinase 1
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Mitogen-Activated Protein Kinase 3
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Mitogen-Activated Protein Kinases
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Neomycin