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Induction of the growth inhibitor IGF-binding protein 3 by p53

L Buckbinder1, R Talbott, S Velasco-Miguel

  • 1Department of Molecular Genetics, Oncology, Bristol-Myers Squibb Pharmaceutical Research Institute, New Jersey 08543-4000, USA.

Nature
|October 19, 1995
PubMed

Insights

The tumor suppressor p53 activates the insulin-like growth factor binding protein 3 (IGF-BP3) gene. This leads to inhibition of insulin-like growth factor 1 (IGF-1) signaling, impacting cell growth and survival.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Signaling

Background:

  • The tumor suppressor p53 plays a crucial role in regulating cell growth, DNA repair, and apoptosis through transcriptional activation of target genes.
  • p53's tumor-suppressor functions are linked to growth regulation, cell cycle progression (e.g., p21/WAF1), DNA repair (e.g., GADD45), and apoptosis (e.g., bax).

Purpose of the Study:

  • To identify novel p53-regulated target genes.
  • To investigate the functional link between p53 and insulin-like growth factor (IGF) signaling pathways.

Main Methods:

  • Differential cloning approach to identify novel p53 target genes.
  • Analysis of IGF-BP3 gene expression and protein secretion in response to wild-type and mutant p53.
  • Assessment of the inhibitory activity of secreted IGF-BP3 on IGF-1 mitogenic signaling.

Main Results:

  • Identified insulin-like growth factor binding protein 3 (IGF-BP3) as a novel p53-regulated target gene.
  • Wild-type p53, but not mutant p53, induced IGF-BP3 gene expression.
  • Induced IGF-BP3 was secreted in an active form capable of inhibiting insulin-like growth factor 1 (IGF-1) mitogenic signaling.

Conclusions:

  • IGF-BP3 is a novel target gene of the tumor suppressor p53.
  • p53-mediated induction of IGF-BP3 links p53 to IGF signaling pathways.
  • This pathway may regulate cellular growth, transformation, and survival through autocrine/paracrine mechanisms.

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