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DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells

  • Authors:
    • Shichuan Tan
    • Juan Zhao
    • Pin Wang
  • View Affiliations / Copyright

    Affiliations: Department of Otorhinolaryngology, Qilu Hospital of Shandong University, National Health Commission (NHC) Key Laboratory of Otorhinolaryngology, Shandong University, Jinan, Shandong 250012, P.R. China
    Copyright: © Tan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 94
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    Published online on: June 30, 2023
       https://doi.org/10.3892/ijo.2023.5542
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Abstract

Polo-like kinases (PLKs) are a family of serine-threonine kinases that exert regulatory effects on diverse cellular processes. Dysregulation of PLKs has been implicated in multiple cancers, including glioblastoma (GBM). Notably, PLK2 expression in GBM tumor tissue is lower than that in normal brains. Notably, high PLK2 expression is significantly correlated with poor prognosis. Thus, it can be inferred that PLK2 expression alone may not be sufficient for accurate prognosis evaluation, and there are unknown mechanisms underlying PLK2 regulation. In the present study, it was demonstrated that dual specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A) interacts with and phosphorylates PLK2 at Ser358. DYRK1A-mediated phosphorylation of PLK2 increases its protein stability. Moreover, PLK2 kinase activity was markedly induced by DYRK1A, which was exemplified by the upregulation of alpha-synuclein S129 phosphorylation. Furthermore, it was found that phosphorylation of PLK2 by DYRK1A contributes to the proliferation, migration and invasion of GBM cells. DYRK1A further enhances the inhibition of the malignancy of GBM cells already induced by PLK2. The findings of the present study indicate that PLK2 may play a crucial role in GBM pathogenesis partially in a DYRK1A-dependent manner, suggesting that PLK2 Ser358 may serve as a therapeutic target for GBM.
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Copy and paste a formatted citation
Spandidos Publications style
Tan S, Zhao J and Wang P: DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells. Int J Oncol 63: 94, 2023.
APA
Tan, S., Zhao, J., & Wang, P. (2023). DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells. International Journal of Oncology, 63, 94. https://doi.org/10.3892/ijo.2023.5542
MLA
Tan, S., Zhao, J., Wang, P."DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells". International Journal of Oncology 63.2 (2023): 94.
Chicago
Tan, S., Zhao, J., Wang, P."DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells". International Journal of Oncology 63, no. 2 (2023): 94. https://doi.org/10.3892/ijo.2023.5542
Copy and paste a formatted citation
x
Spandidos Publications style
Tan S, Zhao J and Wang P: DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells. Int J Oncol 63: 94, 2023.
APA
Tan, S., Zhao, J., & Wang, P. (2023). DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells. International Journal of Oncology, 63, 94. https://doi.org/10.3892/ijo.2023.5542
MLA
Tan, S., Zhao, J., Wang, P."DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells". International Journal of Oncology 63.2 (2023): 94.
Chicago
Tan, S., Zhao, J., Wang, P."DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells". International Journal of Oncology 63, no. 2 (2023): 94. https://doi.org/10.3892/ijo.2023.5542
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