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Article

NFATc1 activation promotes the invasion of U251 human glioblastoma multiforme cells through COX-2

  • Authors:
    • Laizang Wang
    • Zhi Wang
    • Jianhua Li
    • Weiguang Zhang
    • Fubin Ren
    • Wu Yue
  • View Affiliations / Copyright

    Affiliations: Department of Neurosurgery, Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China
  • Pages: 1333-1340
    |
    Published online on: March 4, 2015
       https://doi.org/10.3892/ijmm.2015.2124
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Abstract

Recent studies have revealed that the nuclear factor of activated T-cells (NFAT) is a transcription factor that is highly expressed in aggressive cancer cells and tissues, and mediates invasion through the transcriptional induction of pro-invasion and pro-migration genes. However, the mechanisms through which nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), in particular, translocates to the nucleus and regulates the invasion of human glioblastoma multiforme (GBM) cells have not yet been fully elucidated. In the present study, to investigate the role of NFATc1 in GBM cells, we established a U251 cell line expressing a constitutively active form of NFATc1 (CA-NFATc1). On the other hand, RNA interference was used to knock down NFATc1 expression in the U251 cell line. Our results demonstrated that the expression of CA-NFATc1 promoted cancer cell invasion, while small interfering RNA (siRNA) against NFATc1 successfully inhibited the invasion ability of the U251 cell line. Moreover, we demonstrated that NFATc1 promoted U251 cell invasion through the induction of cyclooxygenase-2 (COX‑2). NFAT transcriptionally regulates the induction of COX-2 induction in U251 cells and binds to the promoter. We also demonstrated that a large proportion of GBM specimens expressed NFATc1. NFATc1 expression increased according to the histopathological grade of the glioma. However, no NFATc1 staining was observed in the non-neoplastic brain tissues. These findings suggest that the inhibition of the activation of the NFATc1 pathway is an effective therapeutic strategy for the clinical management of GBM.
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Copy and paste a formatted citation
Spandidos Publications style
Wang L, Wang Z, Li J, Zhang W, Ren F and Yue W: NFATc1 activation promotes the invasion of U251 human glioblastoma multiforme cells through COX-2. Int J Mol Med 35: 1333-1340, 2015.
APA
Wang, L., Wang, Z., Li, J., Zhang, W., Ren, F., & Yue, W. (2015). NFATc1 activation promotes the invasion of U251 human glioblastoma multiforme cells through COX-2. International Journal of Molecular Medicine, 35, 1333-1340. https://doi.org/10.3892/ijmm.2015.2124
MLA
Wang, L., Wang, Z., Li, J., Zhang, W., Ren, F., Yue, W."NFATc1 activation promotes the invasion of U251 human glioblastoma multiforme cells through COX-2". International Journal of Molecular Medicine 35.5 (2015): 1333-1340.
Chicago
Wang, L., Wang, Z., Li, J., Zhang, W., Ren, F., Yue, W."NFATc1 activation promotes the invasion of U251 human glioblastoma multiforme cells through COX-2". International Journal of Molecular Medicine 35, no. 5 (2015): 1333-1340. https://doi.org/10.3892/ijmm.2015.2124
Copy and paste a formatted citation
x
Spandidos Publications style
Wang L, Wang Z, Li J, Zhang W, Ren F and Yue W: NFATc1 activation promotes the invasion of U251 human glioblastoma multiforme cells through COX-2. Int J Mol Med 35: 1333-1340, 2015.
APA
Wang, L., Wang, Z., Li, J., Zhang, W., Ren, F., & Yue, W. (2015). NFATc1 activation promotes the invasion of U251 human glioblastoma multiforme cells through COX-2. International Journal of Molecular Medicine, 35, 1333-1340. https://doi.org/10.3892/ijmm.2015.2124
MLA
Wang, L., Wang, Z., Li, J., Zhang, W., Ren, F., Yue, W."NFATc1 activation promotes the invasion of U251 human glioblastoma multiforme cells through COX-2". International Journal of Molecular Medicine 35.5 (2015): 1333-1340.
Chicago
Wang, L., Wang, Z., Li, J., Zhang, W., Ren, F., Yue, W."NFATc1 activation promotes the invasion of U251 human glioblastoma multiforme cells through COX-2". International Journal of Molecular Medicine 35, no. 5 (2015): 1333-1340. https://doi.org/10.3892/ijmm.2015.2124
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