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Article

Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway

  • Authors:
    • Dong Li
    • Li-Nan Zhao
    • Xiu-Lan Zheng
    • Ping Lin
    • Feng Lin
    • Yue Li
    • Hai‑Feng Zou
    • Rong-Jun Cui
    • Hui Chen
    • Xiao-Guang Yu
  • View Affiliations / Copyright

    Affiliations: Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China, Department of Ultrasonography, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150081, P.R. China, Department of Urology, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China
  • Pages: 3169-3176
    |
    Published online on: October 13, 2014
       https://doi.org/10.3892/mmr.2014.2630
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Abstract

Prostate cancer is the most commonly diagnosed type of cancer and the second leading cause of cancer‑associated mortality in males. The efficacy of prostate cancer chemotherapy is frequently impaired by drug resistance; however, the underlying mechanisms of this resistance remain elusive. Sex determining region Y-box 2 (Sox2) is of vital importance in the regulation of stem cell proliferation and carcinogenesis. In the present study, using MTT, clone formation, cell cycle and apoptosis assays, over-expression of Sox2 was demonstrated to enhance the paclitaxel (Pac) resistance of the PC-3 prostate cancer cell line, promoting cell proliferation and exhibiting an anti‑apoptotic effect. Western blot analysis revealed that the phosphoinositide 3-kinase/Akt signaling pathway was activated in cells overexpressing Sox2, and by targeting cyclin E and survivin, Sox2 promoted G1/S phase transition and prevented apoptosis under Pac treatment. The present study provided an understanding of Pac resistance in prostate cancer and may indicate novel therapeutic methods for chemoresistant prostate cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Li D, Zhao L, Zheng X, Lin P, Lin F, Li Y, Zou HF, Cui R, Chen H, Yu X, Yu X, et al: Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway. Mol Med Rep 10: 3169-3176, 2014.
APA
Li, D., Zhao, L., Zheng, X., Lin, P., Lin, F., Li, Y. ... Yu, X. (2014). Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway. Molecular Medicine Reports, 10, 3169-3176. https://doi.org/10.3892/mmr.2014.2630
MLA
Li, D., Zhao, L., Zheng, X., Lin, P., Lin, F., Li, Y., Zou, H., Cui, R., Chen, H., Yu, X."Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway". Molecular Medicine Reports 10.6 (2014): 3169-3176.
Chicago
Li, D., Zhao, L., Zheng, X., Lin, P., Lin, F., Li, Y., Zou, H., Cui, R., Chen, H., Yu, X."Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway". Molecular Medicine Reports 10, no. 6 (2014): 3169-3176. https://doi.org/10.3892/mmr.2014.2630
Copy and paste a formatted citation
x
Spandidos Publications style
Li D, Zhao L, Zheng X, Lin P, Lin F, Li Y, Zou HF, Cui R, Chen H, Yu X, Yu X, et al: Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway. Mol Med Rep 10: 3169-3176, 2014.
APA
Li, D., Zhao, L., Zheng, X., Lin, P., Lin, F., Li, Y. ... Yu, X. (2014). Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway. Molecular Medicine Reports, 10, 3169-3176. https://doi.org/10.3892/mmr.2014.2630
MLA
Li, D., Zhao, L., Zheng, X., Lin, P., Lin, F., Li, Y., Zou, H., Cui, R., Chen, H., Yu, X."Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway". Molecular Medicine Reports 10.6 (2014): 3169-3176.
Chicago
Li, D., Zhao, L., Zheng, X., Lin, P., Lin, F., Li, Y., Zou, H., Cui, R., Chen, H., Yu, X."Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway". Molecular Medicine Reports 10, no. 6 (2014): 3169-3176. https://doi.org/10.3892/mmr.2014.2630
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