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Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells
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Modulation of angiogenesis-related protein synthesis by valproic acid

Dimitrios Zgouras1, Ute Becker, Stefan Loitsch

  • 1Second Department of Medicine, Johann Wolfgang Goethe University, Theodor-Stern-Kai 7, D-60590 Frankfurt, Germany.

Biochemical and Biophysical Research Communications
|March 23, 2004
PubMed

Insights

Valproic acid, a histone deacetylase (HDAC) inhibitor, effectively reduces angiogenesis by suppressing key factors like VEGF and FGF in colon carcinoma cells. This suggests its potential as a novel therapeutic agent for colon cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Histone deacetylase (HDAC) inhibitors show antiangiogenic effects on solid tumors.
  • Butyrate, an HDAC inhibitor, impairs tumor-induced angiogenesis but has poor bioavailability.
  • Valproic acid, an HDAC inhibitor, is well-tolerated and bioavailable, with known inhibitory effects on carcinoma cells.

Purpose of the Study:

  • To investigate the antiangiogenic potential of valproic acid.
  • To determine if valproic acid affects angiogenic factors in colon carcinoma cells.

Main Methods:

  • Treatment of Caco-2 cells with valproic acid.
  • Analysis of vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) protein and mRNA levels.
  • Assessment of ubiquitin-proteasome activity.

Main Results:

  • Valproic acid significantly repressed both protein and mRNA levels of VEGF.
  • Valproic acid also reduced FGF levels in Caco-2 cells.
  • Suppression of ubiquitin-proteasome activity may underlie valproic acid's antiangiogenic effects.

Conclusions:

  • Valproic acid demonstrates antiangiogenic properties by inhibiting VEGF and FGF.
  • The drug's favorable bioavailability and tolerability profile make it a promising candidate.
  • Valproic acid may offer a new therapeutic strategy for colon carcinoma treatment.

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