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Updated: Aug 18, 2026

Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells
Published on: July 30, 2020
Aurora kinases, aneuploidy and cancer, a coincidence or a real link?
Régis Giet1, Clotilde Petretti, Claude Prigent
1CNRS UMR6061 Université de Rennes 1, Groupe Cycle Cellulaire, Equipe Labellisée LNCC, Université de Rennes 1, IFR140 GFAS, Faculté de Médecine, 2 Avenue du Pr Léon Bernard, CS 3417, Rennes cedex, France.
Abstract:
As Aurora kinases are overexpressed in a large number of cancers, and ectopic expression of Aurora generates polyploid cells containing multiple centrosomes, it has been tempting to suggest that Aurora overexpression provokes genetic instability underlying the tumorigenesis. However, examination of the evidence suggests a more complex relationship. Overexpression of Aurora-A readily transforms rat-1 and NIH3T3 cells, but not primary cells, whereas overexpression of Aurora-B induces metastasis after implantation of tumors in nude mice. Why do polyploid cells containing abnormal centrosome numbers induced by Aurora not get eliminated at cell-cycle checkpoints? Does this phenotype determine the origin of cancer or does it only promote tumor progression? Would drugs against Aurora family members be of any help for cancer treatment? These and related questions are addressed in this review (which is part of the Chromosome Segregation and Aneuploidy series).
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