A Pin1/mutant p53 axis promotes aggressiveness in breast cancer

Cancer Cell. 2011 Jul 12;20(1):79-91. doi: 10.1016/j.ccr.2011.06.004.

Abstract

TP53 missense mutations dramatically influence tumor progression, however, their mechanism of action is still poorly understood. Here we demonstrate the fundamental role of the prolyl isomerase Pin1 in mutant p53 oncogenic functions. Pin1 enhances tumorigenesis in a Li-Fraumeni mouse model and cooperates with mutant p53 in Ras-dependent transformation. In breast cancer cells, Pin1 promotes mutant p53 dependent inhibition of the antimetastatic factor p63 and induction of a mutant p53 transcriptional program to increase aggressiveness. Furthermore, we identified a transcriptional signature associated with poor prognosis in breast cancer and, in a cohort of patients, Pin1 overexpression influenced the prognostic value of p53 mutation. These results define a Pin1/mutant p53 axis that conveys oncogenic signals to promote aggressiveness in human cancers.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Breast Neoplasms / enzymology*
  • Breast Neoplasms / genetics
  • Breast Neoplasms / pathology*
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Disease Models, Animal
  • Female
  • Gene Expression Regulation, Neoplastic
  • Gene Knock-In Techniques
  • Humans
  • Mice
  • Models, Biological
  • Mutant Proteins / genetics
  • Mutant Proteins / metabolism*
  • NIMA-Interacting Peptidylprolyl Isomerase
  • Neoplasm Invasiveness
  • Peptidylprolyl Isomerase / metabolism*
  • Transcription, Genetic
  • Treatment Outcome
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Mutant Proteins
  • NIMA-Interacting Peptidylprolyl Isomerase
  • Tumor Suppressor Protein p53
  • PIN1 protein, human
  • Peptidylprolyl Isomerase
  • Pin1 protein, mouse

Associated data

  • GEO/GSE26262