title: Aurora-A Kinase as a Promising Therapeutic Target in Cancer.
abstract: Mammalian Aurora family of serine/threonine kinases are master regulators of mitotic progression and are frequently overexpressed in human cancers. Among the three members of the Aurora kinase family (Aurora-A, -B, and -C), Aurora-A and Aurora-B are expressed at detectable levels in somatic cells undergoing mitotic cell division. Aberrant Aurora-A kinase activity has been implicated in oncogenic transformation through the development of chromosomal instability and tumor cell heterogeneity. Recent studies also reveal a novel non-mitotic role of Aurora-A activity in promoting tumor progression through activation of epithelial-mesenchymal transition reprograming resulting in the genesis of tumor-initiating cells. Therefore, Aurora-A kinase represents an attractive target for cancer therapeutics, and the development of small molecule inhibitors of Aurora-A oncogenic activity may improve the clinical outcomes of cancer patients. In the present review, we will discuss mitotic and non-mitotic functions of Aurora-A activity in oncogenic transformation and tumor progression. We will also review the current clinical studies, evaluating small molecule inhibitors of Aurora-A activity and their efficacy in the management of cancer patients.
authors.affiliation: Department of Medical Oncology, Mayo Clinic College of Medicine, Rochester, MN, USA; Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
authors.forename: Antonino B
authors.initials: AB
authors.lastname: D'Assoro
authors.affiliation: Department of Medical Oncology, Mayo Clinic College of Medicine , Rochester, MN , USA.
authors.forename: Tufia
authors.initials: T
authors.lastname: Haddad
authors.affiliation: Department of Medical Oncology, Mayo Clinic College of Medicine, Rochester, MN, USA; Department of Molecular Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA.
authors.forename: Evanthia
authors.initials: E
authors.lastname: Galanis
keywords: cancer; cell cycle; mitotic kinase; targeted therapy; tumor progression