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Protein kinase C regulates ezrin-radixin-moesin phosphorylation in canine osteosarcoma cells

  1. Author:
    Hong, S. H.
    Osborne, T.
    Ren, L.
    Briggs, J.
    Mazcko, C.
    Burkett, S. S.
    Khanna, C.

  2. Author Address

    [Hong, SH; Osborne, T; Ren, L; Briggs, J; Khanna, C] NCI, Tumor & Metastasis Biol Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA. [Mazcko, C; Khanna, C] NCI, Comparat Oncol Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. [Burkett, SS] NCI, Mouse Canc Genet Program, NIH, Frederick, MD 21701 USA.;Hong, SH (reprint author), NCI, Tumor & Metastasis Biol Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, 37 Convent Dr, Bethesda, MD 20892 USA;hongsu@mail.nih.gov
    1. Year: 2011
    2. Date: Sep
  2. Journal: Veterinary and Comparative Oncology
    1. 9
    2. 3
    3. Pages: 207-218
  4. Type of Article: Article
  5. ISSN: 1476-5810
  1. Abstract:

    The development of metastasis is the most significant cause of death for both canine and human patients with osteosarcoma (OS). Ezrin has been associated with tumour progression and metastasis in human, canine and murine OS. Ezrin activation is dynamically regulated by protein kinase C (PKC) during metastatic progression in human and murine OS. To include the dog in the development of therapeutics that target ezrin biology, we characterized four new canine OS cell lines and confirmed the relationship between PKC and ezrin in these cells. Three of four cell lines formed tumours in mice that were histologically consistent with OS. All cell lines were markedly aneuploid and expressed ezrin and PKC. Finally, both ezrin phosphorylation and cell migration were inhibited using a PKC inhibitor. These data suggest that an association between PKC-mediated activation of ezrin and the metastatic phenotype in canine OS cells.

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  2. DOI: 10.1111/j.1476-5829.2010.00249.x
  3. View record in Web of Science®
  4. WOS: 000294020000005

Library Notes

  1. Fiscal Year: FY2011-2012
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