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    Expression of cell cycle regulatory factors in differentiating osteoblasts: postproliferative up-regulation of cyclins B and E

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    Authors
    Smith, Elisheva
    Frenkel, Baruch
    Schlegel, Robert
    Giordano, Antonio
    Lian, Jane B.
    Stein, Janet L.
    Stein, Gary S.
    UMass Chan Affiliations
    Department of Cell Biology and Cancer Center
    Document Type
    Journal Article
    Publication Date
    1995-11-01
    Keywords
    Animals
    Cell Cycle
    Cell Cycle Proteins
    Cell Differentiation
    Cell Division
    Cell Nucleus
    Cells, Cultured
    Cyclins
    Cytoplasm
    Osteoblasts
    Osteosarcoma
    Rats
    Subcellular Fractions
    Transforming Growth Factor beta
    Up-Regulation
    Cancer Biology
    Cell Biology
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    Abstract
    The representation of cyclins and cyclin-dependent kinases (cdks) was analyzed during progressive development of the bone cell phenotype in cultures of normal diploid rat calvarial osteoblasts. Three developmental stages were examined: (a) proliferation; (b) monolayer confluency; and (c) mineralization of the bone extracellular matrix. We demonstrate that the presence of cyclins and cdks is not restricted to the proliferation period. Consistent with their role in cell cycle progression, cdc2 and cdk2 decrease postproliferatively. However, cdk4 and cyclins A, B, and D1 persist in confluent cells. Cyclin E is significantly up-regulated during the extracellular matrix mineralization developmental period. Examination of the cytoplasmic levels of these cell cycle regulatory proteins indicates a marked increase in cyclin B in the late differentiation stage. The elevation of nuclear cyclin E and cytoplasmic cyclin B is not observed in osteoblasts maintained under culture conditions that do not support differentiation. Furthermore, treatment with transforming growth factor beta for 48 h during the proliferation period renders the cells incompetent for differentiation and abrogates the postproliferative up-regulation of cyclins B and E. Density-induced growth inhibition of ROS 17/2.8 osteosarcoma cells is not accompanied by up-regulation of nuclear cyclin E and cytoplasmic cyclin B when compared to the proliferation period. This observation is consistent with abrogation of both growth control and differentiation regulatory mechanisms in tumor cells. These results suggest that cell cycle regulatory proteins function not only during proliferation but may also play a role in normal diploid osteoblast differentiation.
    Source
    Cancer Res. 1995 Nov 1;55(21):5019-24.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/40920
    PubMed ID
    7585545
    Related Resources
    Link to article in PubMed
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    UMass Chan Faculty and Researcher Publications

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