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Article

Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer

  • Authors:
    • Li Cheng
    • Jin Zang
    • Han-Jue Dai
    • Feng Li
    • Feng Guo
  • View Affiliations / Copyright

    Affiliations: Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China, Department of Urology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China, Department of Oncology, Nanjing Medical University Affiliated Suzhou Hospital, Suzhou, Jiangsu 215001, P.R. China
  • Pages: 203-214
    |
    Published online on: April 24, 2018
       https://doi.org/10.3892/ijo.2018.4377
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Abstract

Carboxyl terminus of Hsc-70-interacting protein (CHIP) is an E3 ubiquitin ligase that induces the ubiquitination and degradation of numerous tumor-associated proteins and serves as a suppressor or promoter in tumor progression. To date, the molecular mechanism of CHIP in prostate cancer remains unknown. Therefore, the present study investigated the biological function of CHIP in prostate cancer cells and obtained evidence that CHIP expression is upregulated in prostate cancer tissues. The CHIP vector was introduced into DU145 cancer cells and the cell biological behaviour was examined through a series of experiments, including cell growth, cell apoptosis and migration and invasion assays. The results indicated that the overexpression of CHIP in DU145 prostatic cancer cells promoted cell proliferation through activation of the protein kinase B (AKT) signaling pathway, which subsequently increased cyclin D1 protein levels and decreased p21 and p27 protein levels. The overexpression of CHIP significantly increased the migration and invasion of the DU145 cells, which is possible due to activation of the AKT signaling pathway and upregulation of vimentin. The expression level of CHIP was observed to be increased in human prostate cancer tissues compared with the adjacent normal tissue. Furthermore, the CHIP expression level exhibited a positively association with the Gleason score of the patents. These findings indicate that CHIP functions as an oncogene in prostate cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Cheng L, Zang J, Dai H, Li F and Guo F: Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer. Int J Oncol 53: 203-214, 2018.
APA
Cheng, L., Zang, J., Dai, H., Li, F., & Guo, F. (2018). Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer. International Journal of Oncology, 53, 203-214. https://doi.org/10.3892/ijo.2018.4377
MLA
Cheng, L., Zang, J., Dai, H., Li, F., Guo, F."Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer". International Journal of Oncology 53.1 (2018): 203-214.
Chicago
Cheng, L., Zang, J., Dai, H., Li, F., Guo, F."Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer". International Journal of Oncology 53, no. 1 (2018): 203-214. https://doi.org/10.3892/ijo.2018.4377
Copy and paste a formatted citation
x
Spandidos Publications style
Cheng L, Zang J, Dai H, Li F and Guo F: Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer. Int J Oncol 53: 203-214, 2018.
APA
Cheng, L., Zang, J., Dai, H., Li, F., & Guo, F. (2018). Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer. International Journal of Oncology, 53, 203-214. https://doi.org/10.3892/ijo.2018.4377
MLA
Cheng, L., Zang, J., Dai, H., Li, F., Guo, F."Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer". International Journal of Oncology 53.1 (2018): 203-214.
Chicago
Cheng, L., Zang, J., Dai, H., Li, F., Guo, F."Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer". International Journal of Oncology 53, no. 1 (2018): 203-214. https://doi.org/10.3892/ijo.2018.4377
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