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Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer

  • Authors:
    • Feilun Cui
    • Jianpeng Hu
    • Yu Fan
    • Jian Tan
    • Huaming Tang
  • View Affiliations / Copyright

    Affiliations: Department of Urology, The Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu 212000, P.R. China, Department of Oncology, The Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu 212000, P.R. China
    Copyright: © Cui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5712-5720
    |
    Published online on: February 8, 2018
       https://doi.org/10.3892/ol.2018.8003
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Abstract

Prostate cancer (PCa) is the most frequently diagnosed type of cancer in Chinese males. Cell‑cycle aberration is a hallmark of cancer. Spindle pole body component 25 homolog (SPC25), a component of the Ndc80 complex, serves an important role in regulating mitotic chromosome segregation. However, the functional roles of SPC25 in PCa remain poorly understood. To the best of our knowledge, the present study was the first to demonstrate that SPC25 is significantly upregulated in PCa. In order to investigate the molecular roles of SPC25, a loss of function assay was performed, revealing that SPC25 knockdown inhibited cell proliferation, and induced a decrease in the number of cells in the S phase and an increase in the number of cells in the G2/M phase. Furthermore, SPC25 knockdown promoted the apoptosis of PCa cells. Additionally, bioinformatics analysis revealed multiple functional roles of SPC25 in regulating cell proliferation, apoptosis, invasion, transforming growth factor‑β signaling and the SUMOylation pathway in PCa. The present study also evaluated the potential prognostic value of SPC25 using The Cancer Genome Atlas RNA‑seq data and demonstrated that SPC25 was upregulated in late stage PCa. Kaplan‑Meier analysis demonstrated that lower SPC25 expression was associated with an improved survival rate in patients with PCa. Taken together, these results suggested that SPC25 serves an oncogenic role in PCa and may act as a novel diagnostic and therapeutic target for PCa.
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Copy and paste a formatted citation
Spandidos Publications style
Cui F, Hu J, Fan Y, Tan J and Tang H: Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer. Oncol Lett 15: 5712-5720, 2018.
APA
Cui, F., Hu, J., Fan, Y., Tan, J., & Tang, H. (2018). Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer. Oncology Letters, 15, 5712-5720. https://doi.org/10.3892/ol.2018.8003
MLA
Cui, F., Hu, J., Fan, Y., Tan, J., Tang, H."Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer". Oncology Letters 15.4 (2018): 5712-5720.
Chicago
Cui, F., Hu, J., Fan, Y., Tan, J., Tang, H."Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer". Oncology Letters 15, no. 4 (2018): 5712-5720. https://doi.org/10.3892/ol.2018.8003
Copy and paste a formatted citation
x
Spandidos Publications style
Cui F, Hu J, Fan Y, Tan J and Tang H: Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer. Oncol Lett 15: 5712-5720, 2018.
APA
Cui, F., Hu, J., Fan, Y., Tan, J., & Tang, H. (2018). Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer. Oncology Letters, 15, 5712-5720. https://doi.org/10.3892/ol.2018.8003
MLA
Cui, F., Hu, J., Fan, Y., Tan, J., Tang, H."Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer". Oncology Letters 15.4 (2018): 5712-5720.
Chicago
Cui, F., Hu, J., Fan, Y., Tan, J., Tang, H."Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer". Oncology Letters 15, no. 4 (2018): 5712-5720. https://doi.org/10.3892/ol.2018.8003
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