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Article

Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity

  • Authors:
    • Chunling Fu
    • Yanqing Gong
    • Xuanxuan Shi
    • Hengliang Shi
    • Yan Wan
    • Qingyun Wu
    • Kailin Xu
  • View Affiliations / Copyright

    Affiliations: Blood Diseases Institute, Xuzhou Medical College, Xuzhou, Jiangsu 221002, P.R. China, Department of Neurosurgery, The Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu 221002, P.R. China
  • Pages: 1493-1500
    |
    Published online on: December 28, 2015
       https://doi.org/10.3892/or.2015.4526
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Abstract

Chronic lymphocytic leukemia (CLL) is the most common leukemia in Western countries, and mainly originates from an accumulation of abnormal B cells caused by the dysregulation of cell proliferation and apoptosis. The aberration of proliferation-related gene in CLL cells induces cell arrest at G0/G1 phase, or a small section shows rapid cell growth, which further complicates the pathogenesis of CLL. The constitutively photomorphogenic 1 (COP1), as an E3 ubiquitin ligase, is involved in many biological processes in mammalian cells, but its role in chronic lymphocytic leukemia (CLL) progression remains unclear. In the present study, we analyzed the expression of COP1 in peripheral blood mononuclear cells (PBMCs) from 23 CLL patients and 3 healthy donors. The observed upregulated expression of COP1 in CLL patients was positively correlated with CLL clinical stage and ZAP-70 expression, but not del(13q14) and del(17q-). Overexpression of COP1 significantly promoted cell colony formation and proliferation, especially contributing to the accumulation of cells in S-phase by inhibition of FoxO1 and p21. Moreover, overexpression of COP1 accelerated tumorigenicity of HG3 cells and promoted xenograft growth. Therefore, the present study revealed that COP1 plays an important role in CLL cell proliferation and tumorigenicity, and may be a useful indicator of the chronic lymphocytic leukemia processes.
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Copy and paste a formatted citation
Spandidos Publications style
Fu C, Gong Y, Shi X, Shi H, Wan Y, Wu Q and Xu K: Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity. Oncol Rep 35: 1493-1500, 2016.
APA
Fu, C., Gong, Y., Shi, X., Shi, H., Wan, Y., Wu, Q., & Xu, K. (2016). Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity. Oncology Reports, 35, 1493-1500. https://doi.org/10.3892/or.2015.4526
MLA
Fu, C., Gong, Y., Shi, X., Shi, H., Wan, Y., Wu, Q., Xu, K."Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity". Oncology Reports 35.3 (2016): 1493-1500.
Chicago
Fu, C., Gong, Y., Shi, X., Shi, H., Wan, Y., Wu, Q., Xu, K."Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity". Oncology Reports 35, no. 3 (2016): 1493-1500. https://doi.org/10.3892/or.2015.4526
Copy and paste a formatted citation
x
Spandidos Publications style
Fu C, Gong Y, Shi X, Shi H, Wan Y, Wu Q and Xu K: Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity. Oncol Rep 35: 1493-1500, 2016.
APA
Fu, C., Gong, Y., Shi, X., Shi, H., Wan, Y., Wu, Q., & Xu, K. (2016). Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity. Oncology Reports, 35, 1493-1500. https://doi.org/10.3892/or.2015.4526
MLA
Fu, C., Gong, Y., Shi, X., Shi, H., Wan, Y., Wu, Q., Xu, K."Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity". Oncology Reports 35.3 (2016): 1493-1500.
Chicago
Fu, C., Gong, Y., Shi, X., Shi, H., Wan, Y., Wu, Q., Xu, K."Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity". Oncology Reports 35, no. 3 (2016): 1493-1500. https://doi.org/10.3892/or.2015.4526
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