Abstract
Previous studies have shown aberrant expression of miR-214 in human malignancy. Elevated miR-214 is associated with chemoresistance and metastasis. In this study, we identified miR-214 regulation of ovarian cancer stem cell (OCSC) properties by targeting p53/Nanog axis. Enforcing expression of miR-214 increases, whereas knockdown of miR-214 decreases, OCSC population and self-renewal as well as the Nanog level preferentially in wild-type p53 cell lines. Furthermore, we found that p53 is directly repressed by miR-214 and that miR-214 regulates Nanog through p53. Expression of p53 abrogated miR-214-induced OCSC properties. These data suggest the critical role of miR-214 in OCSC via regulation of the p53-Nanog axis and miR-214 as a therapeutic target for ovarian cancer.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Retracted Publication
MeSH terms
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Cell Line, Tumor
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Female
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Gene Expression Regulation, Neoplastic / genetics
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Gene Knockdown Techniques
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Homeodomain Proteins / genetics
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Homeodomain Proteins / metabolism*
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Humans
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MicroRNAs / genetics
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MicroRNAs / metabolism*
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Nanog Homeobox Protein
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Neoplastic Stem Cells / metabolism*
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Ovarian Neoplasms / genetics
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Ovarian Neoplasms / metabolism*
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Ovarian Neoplasms / therapy
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RNA, Neoplasm / genetics
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RNA, Neoplasm / metabolism*
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Tumor Suppressor Protein p53 / biosynthesis*
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Tumor Suppressor Protein p53 / genetics
Substances
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Homeodomain Proteins
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MIRN214 microRNA, human
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MicroRNAs
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NANOG protein, human
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Nanog Homeobox Protein
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RNA, Neoplasm
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TP53 protein, human
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Tumor Suppressor Protein p53