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Article

Protein phosphatase 1γ regulates the proliferation of human glioma via the NF-κB pathway

  • Authors:
    • Zhen Bao
    • Chengwei Duan
    • Cheng Gong
    • Liang Wang
    • Chaoyan Shen
    • Cheng Wang
    • Gang Cui
  • View Affiliations / Copyright

    Affiliations: Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu, P.R. China, Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, P.R. China
  • Pages: 2916-2926
    |
    Published online on: March 1, 2016
       https://doi.org/10.3892/or.2016.4644
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Abstract

Protein phosphatase 1γ (PP1γ), a member of mammalian protein phosphatases, serine/threonine phosphatases, catalyzes the majority of protein dephosphorylation events and regulates diverse cellular processes, such as neuronal signaling, muscle contraction, glycogen synthesis, and cell proliferation. However, its expression and potential functions in human glioma is unclear. In this study, we detected the high expression of PP1γ and phosphorylated p65 (p-p65) in human glioma tissues. Besides, we demonstrated that upregulation of PP1γ was tightly related to poor 5-year survival via systemic statistical analysis. Employing serum-starved and re-feeding models of U251 and U87MG, we observed the increasing expression of PP1γ and p-p65 were accompanied by the cell proliferation markers cyclin D1 and proliferating cell nuclear antigen (PCNA). Employing depletion-PP1γ models, we found downregulated PP1γ and p-p65 compared with upregulated IκBα, which indicates the inhibition of NF-κB pathway, and flow cytometry analysis confirmed the weakened cell proliferation. Moreover, we found that the translocation of p65 into the nucleus was impaired. Collectively, we identified the positive correlation between upregulation of PP1γ and human glioma cell proliferation and that knock-down of PP1γ alleviated the glioma proliferation by reducing p65 transportation into the nucleus. The results showed that PP1γ could accelerate human glioma proliferation via the NF-κB pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Bao Z, Duan C, Gong C, Wang L, Shen C, Wang C and Cui G: Protein phosphatase 1γ regulates the proliferation of human glioma via the NF-κB pathway. Oncol Rep 35: 2916-2926, 2016.
APA
Bao, Z., Duan, C., Gong, C., Wang, L., Shen, C., Wang, C., & Cui, G. (2016). Protein phosphatase 1γ regulates the proliferation of human glioma via the NF-κB pathway. Oncology Reports, 35, 2916-2926. https://doi.org/10.3892/or.2016.4644
MLA
Bao, Z., Duan, C., Gong, C., Wang, L., Shen, C., Wang, C., Cui, G."Protein phosphatase 1γ regulates the proliferation of human glioma via the NF-κB pathway". Oncology Reports 35.5 (2016): 2916-2926.
Chicago
Bao, Z., Duan, C., Gong, C., Wang, L., Shen, C., Wang, C., Cui, G."Protein phosphatase 1γ regulates the proliferation of human glioma via the NF-κB pathway". Oncology Reports 35, no. 5 (2016): 2916-2926. https://doi.org/10.3892/or.2016.4644
Copy and paste a formatted citation
x
Spandidos Publications style
Bao Z, Duan C, Gong C, Wang L, Shen C, Wang C and Cui G: Protein phosphatase 1γ regulates the proliferation of human glioma via the NF-κB pathway. Oncol Rep 35: 2916-2926, 2016.
APA
Bao, Z., Duan, C., Gong, C., Wang, L., Shen, C., Wang, C., & Cui, G. (2016). Protein phosphatase 1γ regulates the proliferation of human glioma via the NF-κB pathway. Oncology Reports, 35, 2916-2926. https://doi.org/10.3892/or.2016.4644
MLA
Bao, Z., Duan, C., Gong, C., Wang, L., Shen, C., Wang, C., Cui, G."Protein phosphatase 1γ regulates the proliferation of human glioma via the NF-κB pathway". Oncology Reports 35.5 (2016): 2916-2926.
Chicago
Bao, Z., Duan, C., Gong, C., Wang, L., Shen, C., Wang, C., Cui, G."Protein phosphatase 1γ regulates the proliferation of human glioma via the NF-κB pathway". Oncology Reports 35, no. 5 (2016): 2916-2926. https://doi.org/10.3892/or.2016.4644
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