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p53缺失会加重由Aurora-C过表达诱导的多倍体和中心体数量异常。

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

作者信息

Dutertre Stéphanie, Hamard-Péron Elise, Cremet Jean-Yves, Thomas Yann, Prigent Claude

机构信息

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

出版信息

Cell Cycle. 2005 Dec;4(12):1783-7. doi: 10.4161/cc.4.12.2172. Epub 2005 Dec 13.

Abstract

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.

摘要

极光激酶C是极光丝氨酸/苏氨酸激酶家族的第三个成员,仅在哺乳动物中发现。由于极光激酶C在许多不同类型的癌细胞中过度表达,我们决定分析其在人类细胞中过度表达的后果。我们首先研究了在HeLa细胞有丝分裂期和间期过表达的绿色荧光蛋白标记的极光激酶C的亚细胞定位。正如预期的那样,在有丝分裂期间,我们发现极光激酶C模拟了极光激酶B。令人惊讶的是,在少数间期细胞中,我们发现极光激酶C定位于中心体,就像极光激酶A一样。然后我们检查了极光激酶C过度表达产生的表型。基本上,它看起来与其他极光激酶过度表达后观察到的表型相似。我们观察到含有两个以上中心体的多倍体细胞增加。更有趣的是,在缺乏功能性p53的情况下,这种表型会加剧。尽管极光激酶C在体细胞中的生理功能仍有待阐明,但我们的结果,就像另外两种极光激酶一样,提出了极光激酶C在癌症发生和发展中的作用问题,尤其是在存在突变型p53的情况下。

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