Abstract
Abnormal cytokinesis increases the possibility of nuclear fusion in tumor cells. However, the role of microRNAs (miRNAs) in abnormal cytokinesis is unclear. Here, we found that miR-1290 was significantly up-regulated in clinical colon cancer tissues. Up-regulation of miR-1290 postponed cytokinesis and led to the formation of multinucleated cells. KIF13B was a target of miR-1290 that was involved in aberrant cytokinesis. Furthermore, enforced expression of miR-1290 activated the Wnt pathway and increased the reprogramming-related transcript factors c-Myc and Nanog. Our results suggest that up-regulation of miR-1290 in colon cancer cells impaired cytokinesis and affected reprogramming.
Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenoma / genetics
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Adenoma / metabolism
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Adenoma / pathology*
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Base Sequence
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Binding Sites
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Cell Line, Tumor
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Cell Nucleus Division
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Cell Proliferation
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Colonic Neoplasms / genetics
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Colonic Neoplasms / metabolism
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Colonic Neoplasms / pathology*
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Cytokinesis / genetics*
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Gene Expression Regulation, Neoplastic
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Homeodomain Proteins / metabolism
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Humans
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Kinesins / genetics
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Kinesins / metabolism
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MicroRNAs / genetics*
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MicroRNAs / metabolism
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MicroRNAs / physiology
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NF-kappa B / metabolism
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Nanog Homeobox Protein
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Proto-Oncogene Proteins c-akt / metabolism
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Proto-Oncogene Proteins c-myc / metabolism
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RNA Interference
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Transcription, Genetic
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Up-Regulation*
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Wnt Signaling Pathway
Substances
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Homeodomain Proteins
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MIRN1290 microRNA, human
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MYC protein, human
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MicroRNAs
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NANOG protein, human
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NF-kappa B
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Nanog Homeobox Protein
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Proto-Oncogene Proteins c-myc
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Proto-Oncogene Proteins c-akt
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KIF13B protein, human
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Kinesins