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Cell Cycle. 2005 Dec;4(12):1783-7. Epub 2005 Dec 13.

The absence of p53 aggravates polyploidy and centrosome number abnormality induced by Aurora-C overexpression.

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  • 1CNRS UMR6061, Génétique et Développement, Université de Rennes 1, IFR140, Groupe Cycle Cellulaire, Equipe Labellisée Ligue Nationale Contre Le Cancer, Faculté de Médecine, Rennes, France.


Aurora-C is the third member of the aurora serine/threonine kinase family and was found only in mammals. Because Aurora-C is overexpressed in many different types of cancer cells we decided to analyze the consequences of Aurora-C overexpression in human cells. We first investigated the subcellular localization of overexpressed GFP-Aurora-C in mitosis and interphase in HeLa cells. As expected, during mitosis, we found that Aurora-C mimics Aurora-B. Surprisingly, in few interphase cells, we found that Aurora-C localized to the centrosome, like Aurora-A. We then examined the phenotype generated by Aurora-C overexpression. Basically it looked similar to the phenotypes observed after overexpression of the other Aurora kinases. We observed an augmentation of polyploid cells containing more than two centrosomes. More interestingly this phenotype was aggravated in the absence of a functional p53. Although the physiological function of Aurora-C in somatic cells remains to be clarified, our results, just like for the two other Aurora kinases, raised the question of a role of Aurora-C in the development and progression of cancer especially in the presence of mutated p53.

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