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    Loss of miRNA biogenesis induces p19Arf-p53 signaling and senescence in primary cells

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    Authors
    Mudhasani, Rajini R.
    Zhu, Zhiqing
    Hutvagner, Gyorgy
    Eischen, Christine M.
    Lyle, Stephen
    Hall, Lisa L.
    Lawrence, Jeanne B.
    Imbalzano, Anthony N.
    Jones, Stephen N.
    UMass Chan Affiliations
    Department of Cancer Biology
    Department of Biochemistry and Molecular Pharmacology
    Department of Cell Biology
    Document Type
    Journal Article
    Publication Date
    2008-07-02
    Keywords
    Animals
    *Cell Aging
    Cell Proliferation
    Cells, Cultured
    Cyclin-Dependent Kinase Inhibitor p16
    DNA Damage
    Embryo, Mammalian
    Fibroblasts
    Gene Deletion
    Mice
    MicroRNAs
    Ribonuclease III
    *Signal Transduction
    Tumor Suppressor Protein p53
    Cancer Biology
    Cell Biology
    Life Sciences
    Medicine and Health Sciences
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    Abstract
    Dicer, an enzyme involved in microRNA (miRNA) maturation, is required for proper cell differentiation and embryogenesis in mammals. Recent evidence indicates that Dicer and miRNA may also regulate tumorigenesis. To better characterize the role of miRNA in primary cell growth, we generated Dicer-conditional mice. Ablation of Dicer and loss of mature miRNAs in embryonic fibroblasts up-regulated p19(Arf) and p53 levels, inhibited cell proliferation, and induced a premature senescence phenotype that was also observed in vivo after Dicer ablation in the developing limb and in adult skin. Furthermore, deletion of the Ink4a/Arf or p53 locus could rescue fibroblasts from premature senescence induced by Dicer ablation. Although levels of Ras and Myc oncoproteins appeared unaltered, loss of Dicer resulted in increased DNA damage and p53 activity in these cells. These results reveal that loss of miRNA biogenesis activates a DNA damage checkpoint, up-regulates p19(Arf)-p53 signaling, and induces senescence in primary cells.
    Source
    J Cell Biol. 2008 Jun 30;181(7):1055-63. Link to article on publisher's site
    DOI
    10.1083/jcb.200802105
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/39186
    PubMed ID
    18591425
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1083/jcb.200802105
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    UMass Chan Faculty and Researcher Publications

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