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Downmodulation of bFGF-binding protein expression following restoration of p53 function

Z A Sherif1, S Nakai, K F Pirollo

  • 1Department of Oncology, Lombardi Cancer Center, Georgetown University Medical Center, Washington, District of Columbia 20007, USA.

Cancer Gene Therapy
|November 1, 2001
PubMed

Insights

Restoring wild-type p53 function inhibits head and neck squamous cell carcinoma growth. This tumor regression is linked to reduced angiogenesis via down-regulation of fibroblast growth factor binding protein.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Solid tumor growth relies on angiogenesis (new blood vessel formation).
  • Inhibiting tumor neovascularization is a strategy for tumor regression.
  • Restoring wild-type p53 (wtp53) function may impede tumor growth through anti-angiogenic mechanisms.

Purpose of the Study:

  • To investigate the effect of wild-type p53 restoration on head and neck squamous cell carcinoma (HNSCC) growth.
  • To determine the role of wtp53 in regulating angiogenesis in HNSCC.
  • To identify molecular targets mediating wtp53-induced anti-tumor effects.

Main Methods:

  • Adenoviral vector-mediated delivery of wtp53 into HNSCC cells.
  • In vitro cell culture experiments to assess tumor cell growth.
  • In vivo xenograft mouse models to evaluate tumor growth inhibition.
  • Analysis of fibroblast growth factor binding protein (FGF-BP) expression levels.

Main Results:

  • Adenoviral wtp53 transduction significantly inhibited HNSCC cell growth both in vitro and in vivo.
  • Tumor growth inhibition was associated with decreased expression of FGF-BP.
  • FGF-BP down-regulation correlated with reduced activation of basic FGF, an angiogenic factor.

Conclusions:

  • Restoration of wtp53 function can inhibit HNSCC tumor growth.
  • wtp53-induced tumor regression is, in part, mediated by anti-angiogenesis.
  • Down-modulation of FGF-BP is a key mechanism in wtp53-driven anti-angiogenic effects.

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