Crosstalk between Aurora-A and p53: Frequent Deletion or Downregulation of Aurora-A in Tumors from p53 Null Mice

Jian Hua Mao, Di Wu, Jesus Perez-Losada, Tao Jiang, Qian Li, Richard M. Neve, Joe W. Gray, Wei Wen Cai, Allan Balmain

Research output: Contribution to journalArticle

57 Scopus citations

Abstract

The Aurora-A kinase gene is amplified in a subset of human tumors and in radiation-induced lymphomas from p53 heterozygous mice. Normal tissues from p53-/- mice have increased Aurora-A protein levels, but lymphomas from these mice exhibit heterozygous deletions of Aurora-A and/or reduced protein expression. A similar correlation between low p53 levels and Aurora-A gene deletions and expression is found in human breast cancer cell lines. In vitro studies using mouse embryo fibroblasts demonstrate that inhibition of Aurora-A can have either positive or negative effects on cell growth as a function of p53 status. These data have implications for the design of approaches to targeted cancer therapy involving the crosstalk between Aurora-A kinase and p53 pathways.

Original languageEnglish (US)
Pages (from-to)161-173
Number of pages13
JournalCancer Cell
Volume11
Issue number2
DOIs
StatePublished - Feb 13 2007

ASJC Scopus subject areas

  • Oncology
  • Cell Biology
  • Cancer Research

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    Mao, J. H., Wu, D., Perez-Losada, J., Jiang, T., Li, Q., Neve, R. M., Gray, J. W., Cai, W. W., & Balmain, A. (2007). Crosstalk between Aurora-A and p53: Frequent Deletion or Downregulation of Aurora-A in Tumors from p53 Null Mice. Cancer Cell, 11(2), 161-173. https://doi.org/10.1016/j.ccr.2006.11.025