Abstract
Our previous miRNAs profiling study showed that miR-27b was up-regulated in glioma cells compared with H4 low grade astrocytoma cells. However, the main function of miR-27b in glioma in not known yet. The aim of this study was to investigate the expression and function of miR-27b in the pathogenesis of glioma. Real-time PCR showed that miR-27b was up-regulated in glioma samples and glioma cells. Down-regulation of miR-27b triggered growth inhibition, induced apoptosis and inhibited invasion in glioma cells. Furthermore, TOPflash luciferase activity was decreased significantly, while FOPflash luciferase did not change significantly. In addition, Western blot assay showed that STAT3, c-myc and cyclin D1 were knocked down after treatment with miR-27b inhibitor. These findings suggest that aberrantly up-regulated miR-27b may be one of the critical factors that contribute to malignancy in human gliomas.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis
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Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / metabolism
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Brain Neoplasms / genetics
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Brain Neoplasms / metabolism*
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Cell Cycle
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Cell Line, Tumor
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Cell Proliferation
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Cyclin D1 / metabolism
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Gene Expression
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Gene Knockdown Techniques
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Genes, Reporter
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Glioma / genetics
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Glioma / metabolism*
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Humans
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Luciferases, Renilla / biosynthesis
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Luciferases, Renilla / genetics
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MicroRNAs / genetics*
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MicroRNAs / metabolism
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Neoplasm Invasiveness
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Proto-Oncogene Proteins c-myc / metabolism
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STAT3 Transcription Factor / metabolism
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Transcription Factor 4
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Transcription Factors / metabolism
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Up-Regulation
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beta Catenin / metabolism
Substances
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Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
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CCND1 protein, human
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MIRN27 microRNA, human
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MYC protein, human
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MicroRNAs
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Proto-Oncogene Proteins c-myc
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STAT3 Transcription Factor
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STAT3 protein, human
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TCF4 protein, human
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Transcription Factor 4
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Transcription Factors
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beta Catenin
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Cyclin D1
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Luciferases, Renilla