Aurora kinases, aneuploidy and cancer, a coincidence or a real link?

Trends Cell Biol. 2005 May;15(5):241-50. doi: 10.1016/j.tcb.2005.03.004.


As Aurora kinases are overexpressed in a large number of cancers, and ectopic expression of Aurora generates polyploid cells containing multiple centrosomes, it has been tempting to suggest that Aurora overexpression provokes genetic instability underlying the tumorigenesis. However, examination of the evidence suggests a more complex relationship. Overexpression of Aurora-A readily transforms rat-1 and NIH3T3 cells, but not primary cells, whereas overexpression of Aurora-B induces metastasis after implantation of tumors in nude mice. Why do polyploid cells containing abnormal centrosome numbers induced by Aurora not get eliminated at cell-cycle checkpoints? Does this phenotype determine the origin of cancer or does it only promote tumor progression? Would drugs against Aurora family members be of any help for cancer treatment? These and related questions are addressed in this review (which is part of the Chromosome Segregation and Aneuploidy series).

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aneuploidy*
  • Animals
  • Aurora Kinase A
  • Aurora Kinase B
  • Aurora Kinases
  • Cell Cycle
  • Centrosome / enzymology
  • Humans
  • Male
  • Meiosis
  • Mice
  • Models, Biological
  • Neoplasms / enzymology*
  • Neoplasms / etiology
  • Neoplasms / genetics*
  • Oncogenes
  • Ploidies
  • Protein-Serine-Threonine Kinases / genetics*
  • Protein-Serine-Threonine Kinases / physiology*
  • Rats


  • AURKB protein, human
  • Aurka protein, mouse
  • Aurka protein, rat
  • Aurkb protein, mouse
  • Aurkb protein, rat
  • Aurora Kinase A
  • Aurora Kinase B
  • Aurora Kinases
  • Protein-Serine-Threonine Kinases