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CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells

  • Authors:
    • Feng Li
    • Dan Jin
    • Chuanxi Tang
    • Dianshuai Gao
  • View Affiliations / Copyright

    Affiliations: Department of Cell Biology and Neurobiology, Xuzhou Key Laboratory of Neurobiology, Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 4789-4796
    |
    Published online on: February 2, 2018
       https://doi.org/10.3892/ol.2018.7934
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Abstract

Human glioma is one of the major malignancies worldwide with an increased mortality rate. Centrosomal protein of 55 kDa (CEP55) is an essential component of the CEP family and has been identified as a prognostic marker for multiple types of cancer. However, the function of CEP55 during glioma tumorigenesis remains unclear. In the present study, the data derived from the Oncomine database indicated that the expression of CEP55 is increased in glioma tissues compared with normal tissues. Furthermore, the expression of CEP55 was also increased at the level of mRNA and protein in glioma cell lines compared with normal human astrocytes. The knockdown of CEP55 expression inhibited the proliferation of glioma U251 cells, whereas overexpression of CEP55 induced the proliferation of U251 cells. Flow cytometric analysis indicated that the knockdown of CEP55 resulted in an increased number of cells arrested at G2/M phase, and apoptosis was promoted. Further investigations revealed that the overexpression of CEP55 increased the phosphorylation of Akt and inhibited the activity of p21. By contrast, the knockdown of CEP55 resulted in the opposite effects. Taken together, the results of the present study suggested that CEP55 regulated the proliferation of glioma cells, further attributing to the carcinogenesis and progression of glioma via the PI3K/Akt/p21 signaling pathway. Therefore, CEP55 may be a novel therapeutic target for the treatment of glioma.
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Copy and paste a formatted citation
Spandidos Publications style
Li F, Jin D, Tang C and Gao D: CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells. Oncol Lett 15: 4789-4796, 2018.
APA
Li, F., Jin, D., Tang, C., & Gao, D. (2018). CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells. Oncology Letters, 15, 4789-4796. https://doi.org/10.3892/ol.2018.7934
MLA
Li, F., Jin, D., Tang, C., Gao, D."CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells". Oncology Letters 15.4 (2018): 4789-4796.
Chicago
Li, F., Jin, D., Tang, C., Gao, D."CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells". Oncology Letters 15, no. 4 (2018): 4789-4796. https://doi.org/10.3892/ol.2018.7934
Copy and paste a formatted citation
x
Spandidos Publications style
Li F, Jin D, Tang C and Gao D: CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells. Oncol Lett 15: 4789-4796, 2018.
APA
Li, F., Jin, D., Tang, C., & Gao, D. (2018). CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells. Oncology Letters, 15, 4789-4796. https://doi.org/10.3892/ol.2018.7934
MLA
Li, F., Jin, D., Tang, C., Gao, D."CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells". Oncology Letters 15.4 (2018): 4789-4796.
Chicago
Li, F., Jin, D., Tang, C., Gao, D."CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells". Oncology Letters 15, no. 4 (2018): 4789-4796. https://doi.org/10.3892/ol.2018.7934
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