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The p53 tumor-suppressor gene is the most frequent target of genetic alterations in human cancer. Numerous studies have demonstrated that the loss of p53 function results in genetic instability, such as mutation, chromosomal translocation, and aneuploidy. It has been shown that the loss of p53 function leads to an abnormal centrosome amplification because of the deregulation of the centrosome duplication cycle. As shown in Figure 1a, centrosome hyperamplification (stained with anti-γ-tubulin antibody; red) was frequently observed in p53-deficient (p53 ) mouse embryonic fibroblasts (MEFs) at interphase. During mitosis, centrosomes form spindle poles and play a vital role in bipolar spindle formation and accurate chromosomal segregation (Fig. 1b). In contrast, the mitotic p53 MEFs frequently displayed aberrant spindles, organized by multiple copies of

Abnormal Centrosome Amplification and Aurora-A Activation in p53-deficient Cells