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Updated: Mar 15, 2026

Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells
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Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells

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The Unexpected Roles of Aurora A Kinase in Gliobastoma Recurrences

Estelle Willems1, Arnaud Lombard1,2, Matthias Dedobbeleer1

  • 1Laboratory of Nervous System Diseases and Therapy, GIGA-Neurosciences, University of Liège, Liège, Belgium.

Targeted Oncology
|August 31, 2016
PubMed

Insights

Glioblastoma (GBM) frequently recurs due to GBM-Initiating Cells (GIC). This review hypothesizes that Aurora A (AurA) kinase activity in GIC drives GBM recurrence and therapeutic resistance.

Area of Science:

  • Neuro-oncology
  • Cancer Biology
  • Molecular Medicine

Background:

  • Glioblastoma (GBM) is characterized by high rates of tumor recurrence, necessitating novel therapeutic strategies.
  • GBM recurrence is linked to Glioblastoma-Initiating Cells (GIC), which possess self-renewal, proliferation, and differentiation capabilities.
  • The mitotic kinase Aurora A (AurA) is implicated in regulating GIC properties and cellular processes contributing to therapeutic resistance.

Purpose of the Study:

  • To review the potential role of Aurora A (AurA) in Glioblastoma-Initiating Cells (GIC).
  • To explore how AurA's functions may contribute to glioblastoma recurrence and therapeutic resistance.

Main Methods:

  • Literature review and synthesis of existing research on Aurora A (AurA) and Glioblastoma-Initiating Cells (GIC).
  • Analysis of AurA's known functions beyond mitosis, including cell polarity and epithelial-to-mesenchymal transition.
  • Hypothesis formulation based on the integration of current knowledge.

Main Results:

  • Aurora A (AurA) kinase regulates key cellular processes implicated in Glioblastoma (GBM) recurrence.
  • AurA's non-mitotic functions, such as regulating cell polarity and asymmetric cell division, may be critical for Glioblastoma-Initiating Cell (GIC) maintenance.
  • These AurA-mediated functions could explain GBM's therapeutic resistance and propensity for relapse.

Conclusions:

  • Aurora A (AurA) is a potential key driver of Glioblastoma (GBM) recurrence by modulating Glioblastoma-Initiating Cells (GIC).
  • Targeting AurA in GIC represents a promising therapeutic avenue to overcome GBM treatment failure and prevent relapse.

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