Targeting Aurora-2 kinase in cancer.

Abstract

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.

• Authors: Steven L Warner, David J Bearss, Haiyong Han, Daniel D Von Hoff
• Journal: Molecular cancer therapeutics (Mol Cancer Ther) Vol. 2 Issue 6 Pg. 589-95 (Jun 2003) ISSN: 1535-7163 [Print] United States
• PMID: 12813139 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S., Review)

Chemical References

• Antineoplastic Agents
• CCNB1 protein, human
• Cyclin B
• Cyclin B1
• RNA, Messenger
• Aurora Kinases
• Protein Serine-Threonine Kinases

Topics

• Antineoplastic Agents (pharmacology)
• Aurora Kinases
• Centrosome (ultrastructure)
• Cyclin B (metabolism)
• Cyclin B1
• Gene Expression Regulation, Neoplastic
• Mitosis
• Models, Biological
• Neoplasms (enzymology)
• Protein Biosynthesis
• Protein Serine-Threonine Kinases (antagonists & inhibitors, genetics, physiology)
• RNA, Messenger (metabolism)