Abstract
To identify microRNAs regulated by oncogenic Notch signaling, we performed microarray-based miRNA profiling of T-cell acute lymphoblastic leukemia (T-ALL) cells before and after treatment with γ-secretase inhibitor (GSI) to block Notch signaling. We show miR-223 levels increase after GSI treatment suggesting that active Notch signaling represses miR-223 expression. We also demonstrate that insulin-like growth factor-1 receptor (IGF1R) is regulated by miR-223 in this context, but observe no apparent effects on cell growth by overexpression or knock-down of miR-223 alone. We conclude that miR-223 contributes to IGF1R regulation, but may act in concert with other genes and/or microRNAs to alter T-ALL biology.
Crown Copyright © 2012. Published by Elsevier Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line, Tumor
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Cell Proliferation
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Down-Regulation / genetics
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Down-Regulation / physiology
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Gene Expression Profiling
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Gene Expression Regulation, Leukemic
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HEK293 Cells
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Humans
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MicroRNAs / genetics*
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MicroRNAs / physiology
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Microarray Analysis
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics*
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology
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Receptor, IGF Type 1 / genetics*
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Receptor, IGF Type 1 / metabolism
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Receptor, Notch1 / genetics
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Receptor, Notch1 / metabolism
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Receptor, Notch1 / physiology*
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Transfection
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Validation Studies as Topic
Substances
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MIRN223 microRNA, human
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MicroRNAs
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NOTCH1 protein, human
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Receptor, Notch1
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Receptor, IGF Type 1