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Article

Overexpression of sigma‑1 receptor in MCF‑7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway

  • Authors:
    • Yuqi Wu
    • Xueyan Bai
    • Xiaoyang Li
    • Chang Zhu
    • Zachary P. Wu
  • View Affiliations / Copyright

    Affiliations: Department of Pharmacy, College of Life Science, China Jiliang University, Hangzhou, Zhejiang 310018, P.R. China
  • Pages: 6763-6769
    |
    Published online on: September 18, 2018
       https://doi.org/10.3892/ol.2018.9448
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Abstract

Sigma‑1 receptor (sigma‑1R), a 25‑kDa integral membrane protein, is expressed at a high density in various tumor cell lines and its ligands mediate tumor cell proliferation. However, the effect of this receptor on proliferation and the associated intracellular molecules in tumors remains unclear. The present study aimed to investigate the effect of sigma‑1R overexpression on MCF‑7 cell proliferation and the associated intracellular molecules that serve a key role in this process. The sigma‑1R proliferative function was examined by comparing the proliferation rates of a sigma‑1R‑overexpressing line, MCF‑41 with a sigma‑1R‑defective line, MCF‑7, in culture media with various serum concentrations. The results demonstrated that MCF‑41 cells grew significantly faster compared with MCF‑7 cells, indicating a proliferation‑enhancing receptor function. This proliferation‑enhancing effect was completely eliminated by adding a PKC inhibitor to the culture media for MCF‑41 cells. To identify which PKC subtype affects the proliferative function of sigma‑1R, five inhibitors of PKC subtypes or enzymes involved in the PKC signaling cascade were introduced to MCF‑7 and MCF‑41 cell culture media and their effects on cell proliferation were compared. It was revealed that only the classic PKC subtype inhibitor, GF109203x, significantly inhibited MCF‑41 cell proliferation compared with the MCF‑7 line. In conclusion, among PKC iso‑enzymes only classic PKC subtype enzymes serve an important role in sigma‑1R overexpression enhancing MCF‑7 cell proliferation.
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Copy and paste a formatted citation
Spandidos Publications style
Wu Y, Bai X, Li X, Zhu C and Wu ZP: Overexpression of sigma‑1 receptor in MCF‑7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway. Oncol Lett 16: 6763-6769, 2018.
APA
Wu, Y., Bai, X., Li, X., Zhu, C., & Wu, Z.P. (2018). Overexpression of sigma‑1 receptor in MCF‑7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway. Oncology Letters, 16, 6763-6769. https://doi.org/10.3892/ol.2018.9448
MLA
Wu, Y., Bai, X., Li, X., Zhu, C., Wu, Z. P."Overexpression of sigma‑1 receptor in MCF‑7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway". Oncology Letters 16.5 (2018): 6763-6769.
Chicago
Wu, Y., Bai, X., Li, X., Zhu, C., Wu, Z. P."Overexpression of sigma‑1 receptor in MCF‑7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway". Oncology Letters 16, no. 5 (2018): 6763-6769. https://doi.org/10.3892/ol.2018.9448
Copy and paste a formatted citation
x
Spandidos Publications style
Wu Y, Bai X, Li X, Zhu C and Wu ZP: Overexpression of sigma‑1 receptor in MCF‑7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway. Oncol Lett 16: 6763-6769, 2018.
APA
Wu, Y., Bai, X., Li, X., Zhu, C., & Wu, Z.P. (2018). Overexpression of sigma‑1 receptor in MCF‑7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway. Oncology Letters, 16, 6763-6769. https://doi.org/10.3892/ol.2018.9448
MLA
Wu, Y., Bai, X., Li, X., Zhu, C., Wu, Z. P."Overexpression of sigma‑1 receptor in MCF‑7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway". Oncology Letters 16.5 (2018): 6763-6769.
Chicago
Wu, Y., Bai, X., Li, X., Zhu, C., Wu, Z. P."Overexpression of sigma‑1 receptor in MCF‑7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway". Oncology Letters 16, no. 5 (2018): 6763-6769. https://doi.org/10.3892/ol.2018.9448
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