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Targeting Aurora-2 Kinase in Cancer¹

Arizona Cancer Center, University of Arizona, Tucson, Arizona 85724

² To whom requests for reprints should be addressed, at Arizona Cancer Center, University of Arizona, P. O. Box 245024, Tucson, AZ 85724-5024. Phone: (520) 626-7925; Fax: (520) 626-6898; E-mail: dvonhoff{at}azcc.arizona.edu

Aurora-2 kinase has been shown to contribute to oncogenic transformation and is frequently overexpressed and amplified in many human tumor types. Aurora-2 belongs to a small family of mitotic serine/threonine kinases that regulate centrosome maturation, chromosome segregation, and cytokinesis. The mechanism behind the transforming activity of aurora-2 is not fully understood; however, the role of aurora-2 in regulating the centrosome cycle is likely responsible for its ability to transform cells. Aurora-2 overexpression has been correlated with centrosome amplification, which can be a driving cause of genomic instability in tumor cells. In addition, recent work has demonstrated that aurora-2 plays an active function in promoting entry into mitosis by regulating local translation of centrosomal stored mRNA, such as cyclin B1. These recent findings implicate aurora-2 as an important regulator of both genomic integrity and cell cycle progression in cancer cells and suggest that aurora-2 is an attractive target for anticancer drug development.

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