Aurora kinases, aneuploidy and cancer, a coincidence or a real link?

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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Trends in Cell Biology, Elsevier, 2005, 15 (5), pp.241-50. 〈10.1016/j.tcb.2005.03.004〉
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Contributeur : Claude Prigent <>
Soumis le : mercredi 26 mars 2014 - 18:07:15
Dernière modification le : mercredi 16 mai 2018 - 11:22:34

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Régis Giet, Clotilde Petretti, Claude Prigent. Aurora kinases, aneuploidy and cancer, a coincidence or a real link?. Trends in Cell Biology, Elsevier, 2005, 15 (5), pp.241-50. 〈10.1016/j.tcb.2005.03.004〉. 〈inserm-00966568〉

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