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 Gray, Wei Wen Cai, Allan Balmain

Research output: Contribution to journalArticle

56 Citations (Scopus)

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
Externally publishedYes

Fingerprint

Down-Regulation
Aurora Kinase A
Lymphoma
Neoplasms
Gene Deletion
Proteins
Embryonic Structures
Fibroblasts
Radiation
Breast Neoplasms
Gene Expression
Cell Line
Growth
Genes
Therapeutics

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Oncology

Cite this

Mao, J. H., Wu, D., Perez-Losada, J., Jiang, T., Li, Q., Neve, R. M., ... 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

Crosstalk between Aurora-A and p53 : Frequent Deletion or Downregulation of Aurora-A in Tumors from p53 Null Mice. / Mao, Jian Hua; Wu, Di; Perez-Losada, Jesus; Jiang, Tao; Li, Qian; Neve, Richard M.; Gray, Joe; Cai, Wei Wen; Balmain, Allan.

In: Cancer Cell, Vol. 11, No. 2, 13.02.2007, p. 161-173.

Research output: Contribution to journalArticle

Mao, JH, Wu, D, Perez-Losada, J, Jiang, T, Li, Q, Neve, RM, Gray, J, Cai, WW & Balmain, A 2007, 'Crosstalk between Aurora-A and p53: Frequent Deletion or Downregulation of Aurora-A in Tumors from p53 Null Mice', Cancer Cell, vol. 11, no. 2, pp. 161-173. https://doi.org/10.1016/j.ccr.2006.11.025
Mao, Jian Hua ; Wu, Di ; Perez-Losada, Jesus ; Jiang, Tao ; Li, Qian ; Neve, Richard M. ; Gray, Joe ; Cai, Wei Wen ; Balmain, Allan. / Crosstalk between Aurora-A and p53 : Frequent Deletion or Downregulation of Aurora-A in Tumors from p53 Null Mice. In: Cancer Cell. 2007 ; Vol. 11, No. 2. pp. 161-173.
@article{3ee50a6ccbe84484bf1fa408b8a202e4,
title = "Crosstalk between Aurora-A and p53: Frequent Deletion or Downregulation of Aurora-A in Tumors from p53 Null Mice",
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.",
author = "Mao, {Jian Hua} and Di Wu and Jesus Perez-Losada and Tao Jiang and Qian Li and Neve, {Richard M.} and Joe Gray and Cai, {Wei Wen} and Allan Balmain",
year = "2007",
month = "2",
day = "13",
doi = "10.1016/j.ccr.2006.11.025",
language = "English (US)",
volume = "11",
pages = "161--173",
journal = "Cancer Cell",
issn = "1535-6108",
publisher = "Cell Press",
number = "2",

}

TY - JOUR

T1 - Crosstalk between Aurora-A and p53

T2 - Frequent Deletion or Downregulation of Aurora-A in Tumors from p53 Null Mice

AU - Mao, Jian Hua

AU - Wu, Di

AU - Perez-Losada, Jesus

AU - Jiang, Tao

AU - Li, Qian

AU - Neve, Richard M.

AU - Gray, Joe

AU - Cai, Wei Wen

AU - Balmain, Allan

PY - 2007/2/13

Y1 - 2007/2/13

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=33846811519&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33846811519&partnerID=8YFLogxK

U2 - 10.1016/j.ccr.2006.11.025

DO - 10.1016/j.ccr.2006.11.025

M3 - Article

C2 - 17292827

AN - SCOPUS:33846811519

VL - 11

SP - 161

EP - 173

JO - Cancer Cell

JF - Cancer Cell

SN - 1535-6108

IS - 2

ER -