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AIMP3 haploinsufficiency disrupts oncogene-induced p53 activation and genomic stability

Bum-Joon Park1, Young Sun Oh, Seung Yong Park

  • 1National Creative Research Initiatives Center for ARS Network, College of Pharmacy, Seoul National University, Seoul, Korea and Institute for Cell and Molecular Pathology, Hannover Medical School, Hannover, Germany.

Cancer Research
|July 20, 2006
PubMed

Insights

Aminoacyl-tRNA synthetase complex-interacting multifunctional protein 1 (AIMP3) prevents cell transformation by coupling oncogenic stresses to p53 activation. Loss of AIMP3 function increases susceptibility to cancer development and genomic instability.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • AIMP3 (p18) is known to up-regulate p53 in response to DNA damage.
  • The role of AIMP3 in preventing oncogene-induced cell transformation is not fully understood.

Purpose of the Study:

  • To investigate the role of AIMP3 in coupling oncogenic stresses to p53 activation.
  • To determine how AIMP3 loss affects cell transformation and genomic stability.

Main Methods:

  • Gene knockout and knockdown studies in cell lines.
  • Oncogene induction assays (Ras, Myc).
  • Analysis of cell division and chromosomal structure.

Main Results:

  • AIMP3 loss or suppression blocked growth factor- or Ras-dependent p53 induction.
  • AIMP3 heterozygous cells were susceptible to transformation by oncogenes like Ras or Myc.
  • Transformed AIMP3+/- cells exhibited severe abnormalities in cell division and chromosomal structure.

Conclusions:

  • AIMP3 is crucial for p53-mediated tumor suppression against oncogenic stress.
  • AIMP3 regulates both ATM and ATR pathways for p53 activation.
  • AIMP3 maintains genomic stability and prevents cell transformation.

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