Abstract
miRNA-21 (miR-21) is overexpressed in various human cancers. Here, we show that miR-21 is overexpressed in human Non-Small Cell Lung Cancer (NSCLC) and that its up or down-regulation, respectively, increases or decreases cyclin D1 and cyclin E1 expression and coordinately promotes or inhibits proliferation of cancer cells. The perturbations of miR-21 also dramatically reduces or increases epithelial to mesenschymal transition (EMT). We show that regulation of proliferation and EMT are directed by PTEN/Akt/GSK3 beta signaling axis by regulating the expression of invasion markers including E-cadherin, vimentin, snail, slug and beta-catenin. Together, these findings show that miR-21 is a potential target for the development of treatment for NSCLC forms of human lung cancer.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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A549 Cells
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Biomarkers, Tumor / genetics
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Biomarkers, Tumor / metabolism
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Carcinoma, Non-Small-Cell Lung / genetics*
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Carcinoma, Non-Small-Cell Lung / metabolism
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Carcinoma, Non-Small-Cell Lung / pathology
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Cell Line, Tumor
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Cell Proliferation / genetics*
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Cyclins / genetics
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Cyclins / metabolism
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Epithelial-Mesenchymal Transition / genetics*
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Gene Expression Regulation, Neoplastic*
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Glycogen Synthase Kinase 3 beta / genetics
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Glycogen Synthase Kinase 3 beta / metabolism
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Humans
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Lung Neoplasms / genetics*
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Lung Neoplasms / metabolism
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Lung Neoplasms / pathology
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MicroRNAs / genetics*
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PTEN Phosphohydrolase / genetics
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PTEN Phosphohydrolase / metabolism
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / metabolism
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Signal Transduction / genetics*
Substances
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Biomarkers, Tumor
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Cyclins
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MIRN21 microRNA, human
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MicroRNAs
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Glycogen Synthase Kinase 3 beta
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Proto-Oncogene Proteins c-akt
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PTEN Phosphohydrolase
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PTEN protein, human