Overexpression of aurora kinase A in mouse mammary epithelium induces genetic instability preceding mammary tumor formation

Aurora A overexpression induces cellular senescence in mammary gland hyperplastic tumors developed in p53-deficient mice

“…In our present study, Aurora A was stably expressed but did not lead to the development of malignant tumors because of the induction of cellular senescence. In contrast, Wang et al (2006) reported recently that overexpression of Aurora A could cause mammary tumor formation through inducing genetic instability and activating AKT. The discrepancy between their results and ours may stem from the use of different mouse strains.…”

“…The discrepancy between their results and ours may stem from the use of different mouse strains. The FVB/N mice used by Wang et al (2006) are highly susceptible to chemically induced squamous cell carcinomas, with a high rate of malignant conversion from papilloma to carcinoma. The different genetic backgrounds of this mouse strain, perhaps, impairment of factors associated with senescence and apoptosis, could result in different outcome of tumorigenesis.…”

Genetic instability and mammary tumor formation in mice carrying mammary-specific disruption of Chk1 and p53

“…Chromosome tetraploidization frequently occurs before aneuploidy during tumorigenesis (Margolis, 2005). It also occurs in mammary cancers developed in transgenic mice with overexpression of oncogenes, such as Aurora-A (Wang et al, 2006). We suspect that the failure of cytokinesis in the Chk1 mutant cells could be, in part, responsible for this phenotype.…”

RASSF1A interacts with and activates the mitotic kinase Aurora-A

“…However, the same regimen did not transform primary murine embryonic fibroblasts (MEFs), suggesting that upregulation of Aurora-A itself is insufficient for oncogenesis (Anand et al, 2003). It is still unclear whether overexpression of Aurora-A induces mammary tumors in transgenic mouse models Wang et al, 2006). Being a multifunctional protein, it is not known which function of Aurora-A contributes to its oncogenic activity.…”