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p53 status in stromal fibroblasts modulates tumor growth in an SDF1-dependent manner

Yoseph Addadi1, Neta Moskovits, Dorit Granot

  • 1Department of Biological Regulation, The Weizmann Institute, Rehovot, Israel.

Cancer Research
|October 19, 2010
PubMed

Insights

The p53 tumor suppressor protein (p53) normally inhibits tumor growth. Loss of p53 in surrounding stromal cells enhances prostate cancer growth and metastasis, suggesting a novel tumor suppressor role for p53.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The p53 tumor suppressor protein (p53) is crucial for preventing tumor development through cell-autonomous functions.
  • Emerging evidence suggests p53 also plays a role in cell nonautonomous tumor suppression.

Purpose of the Study:

  • To investigate the impact of stromal p53 on tumor growth and metastasis.
  • To elucidate the mechanisms by which stromal p53 influences tumor progression.

Main Methods:

  • Utilized PC3 prostate cancer cells and genetically modified fibroblasts with varying p53 statuses (p53-null, p53-mutant).
  • Assessed tumor growth and metastatic spread in a preclinical model.
  • Quantified chemokine expression, specifically SDF-1, in fibroblasts.

Main Results:

  • Ablation of p53 in fibroblasts significantly promoted PC3 tumor growth.
  • This promotion was linked to increased expression of the chemokine SDF-1 in p53-deficient fibroblasts.
  • Fibroblasts expressing mutant p53 were more effective at promoting tumor growth than p53-null fibroblasts.
  • Loss or mutation of p53 in stromal fibroblasts markedly increased tumor metastasis.

Conclusions:

  • p53 acts as a cell nonautonomous tumor suppressor in stromal fibroblasts by inhibiting the production of tumor-promoting factors like SDF-1.
  • Mutant p53 in stromal fibroblasts may confer a gain-of-function advantage, accelerating tumor development and metastasis.

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