Biology of Aurora A kinase: implications in cancer manifestation and therapy

Med Res Rev. 2011 Sep;31(5):757-93. doi: 10.1002/med.20203. Epub 2010 Mar 1.


The Aurora A kinase belongs to serine/threonine group of kinases, well known for its role in cell cycle, especially in the regulation of mitosis. Numerous substrates of Aurora A kinase have been identified, which are predominantly related to cell cycle progression while some of them are transcription factors. Aurora A-mediated phosphorylation can either directly or indirectly regulate the function of its substrates. There are overwhelming evidences which report overexpression and gene amplification of Aurora A in several human cancers, and suggest that Aurora A could be a bona fide oncogene involved in tumorigenesis. Hence, Aurora A plays wide-ranging roles in both mitosis and its deregulation manifests in cancer progression. These observations have favored the choice of Aurora kinases as a target for cancer therapy. Recently, numerous small molecules have been discovered against Aurora kinases and many have entered clinical trials. Most of these small-molecule modulators designed are specific against either Aurora A or Aurora B, but some are dual inhibitors targeting the ATP-binding site which is highly conserved among the three human homologues of Aurora kinase. In this review, we discuss the physiological functions of Aurora A, interactions between Aurora A kinase and its cellular substrates, tumorigenesis mediated by Aurora A kinase upon overexpression, and small-molecule modulators of Aurora kinase as targets for cancer therapy.

Keywords: centrosome dynamics; checkpoint; kinase inhibitors; phosphorylation; tumorigenesis.

Publication types

  • Review

MeSH terms

  • Animals
  • Aurora Kinase A / antagonists & inhibitors
  • Aurora Kinase A / chemistry
  • Aurora Kinase A / genetics
  • Aurora Kinase A / physiology*
  • Gene Expression Regulation, Enzymologic
  • Genes, Tumor Suppressor
  • Genomic Instability
  • Humans
  • Neoplasms / diagnosis
  • Neoplasms / drug therapy
  • Neoplasms / etiology*
  • Polymorphism, Genetic
  • Protein Kinase Inhibitors / therapeutic use
  • Signal Transduction / physiology


  • Protein Kinase Inhibitors
  • Aurora Kinase A