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Modulation of transforming growth factor beta 1 effects on prostate cancer cell proliferation by growth factors and

D M Morton1, E R Barrack

  • 1Department of Urology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-2101, USA.

Cancer Research
|June 15, 1995
PubMed

Insights

Transforming growth factor-beta 1 (TGF-β1) inhibits prostate cancer cell growth in vitro under specific conditions. However, prostate cancer cells develop resistance to TGF-β1

Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Research

Background:

  • Poorly differentiated MATLyLu rat prostate cancer cells exhibit resistance to TGF-β1's growth inhibition in vivo.
  • These cells are sensitive to TGF-β1 in vitro, but only under specific experimental conditions.

Purpose of the Study:

  • To investigate the factors influencing the differential response of prostate cancer cells to TGF-β1 in vitro and in vivo.
  • To understand the mechanisms by which prostate cancer cells evade TGF-β1-mediated growth inhibition.

Main Methods:

  • MATLyLu rat prostate cancer cells were cultured in vitro under varying conditions (cell density, serum concentration, presence of growth factors, extracellular matrix).
  • Cell proliferation was measured in response to different concentrations of TGF-β1.
  • Cell motility was assessed in the presence of TGF-β1.

Main Results:

  • TGF-β1 inhibited proliferation only at low cell density in serum-free medium (IC50 = 0.1 ng/ml).
  • Inhibition was blunted by high cell density, serum, basic fibroblast growth factor, epidermal growth factor, and extracellular matrix.
  • TGF-β1 stimulated cell motility even at high cell density.

Conclusions:

  • Factors like cell density, serum, growth factors, and extracellular matrix explain the in vivo resistance of prostate cancer cells to TGF-β1.
  • Prostate cancer cells retain sensitivity to TGF-β1 but have mechanisms to protect against its growth inhibitory effects in vivo.
  • TGF-β1 may promote tumor aggressiveness by stimulating cell motility, independent of proliferation.

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