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Updated: Apr 30, 2026

Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells
Published on: July 30, 2020
Targeting aurora kinase A inhibits hypoxia-mediated neuroblastoma cell tumorigenesis
Carmelle V Romain1, Pritha Paul, Sora Lee
1Department of Pediatric Surgery, 2200 Children's Way, DOT 7100, Vanderbilt University Medical Center, Nashville, TN 37232-9780, U.S.A. dai.chung@vanderbilt.edu.
Background/Aim:
It is unknown whether hypoxia regulates aurora kinase A (AURKA), a serine/threonine kinase, in neuroblastoma to stimulate cell growth or migration. We sought to determine whether AURKA mediates hypoxia-induced regulation of neuroblastoma tumorigenicity.
Materials And Methods:
Human neuroblastoma BE(2)-C cells were treated with CoCl2, a chemical hypoxia mimetic, and MLN8237, a pharmalogical inhibitor of AURKA, to assess cell viability, colony formation and transwell migration. Focal adhesion kinase (FAK) expression was analyzed after silencing of AURKA under normoxic vs. hypoxic conditions.
Results:
Hypoxia up-regulated expression of AURKA mRNA and protein. CoCl2 stimulated cell proliferation and migration, while inhibiting colony formation. MLN8237 reduced colony formation and cell migration. Silencing of AURKA reduced expression of FAK and pFAK under normoxia and hypoxia.
Conclusion:
Hypoxia positively regulates AURKA expression. Hypoxia-induced stimulation of colony formation and migration is, in part, mediated by AURKA. These findings establish that AURKA is a critical regulator of hypoxia-mediated tumor progression in neuroblastoma.
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