Inhibition of trichostatin A-induced antiangiogenesis by small-interfering RNA for thrombospondin-1

Exp Mol Med. 2007 Jun 30;39(3):402-11. doi: 10.1038/emm.2007.45.

Abstract

Expression of thrombospondin-1 (TSP-1), which is a known inhibitor of tumor growth and angiogenesis, is reciprocally regulated by positive regulators, such as VEGF. Additionally, trichostatin A (TSA) suppresses tumor progression by altering VEGF levels and VEGF-mediated signaling. Thus, understanding TSA-regulated TSP-1 expression and the effects of altered TSP-1 levels might provide insights into the mechanism of action of TSA in anti-tumorigenesis, and provide an approach to cancer therapy. Here, we examined the effect of TSA on TSP-1 expression, and the effects of TSA-induced TSP-1 on cell motility and angiogenesis, in HeLa and bovine aortic endothelial cells. TSA remarkably increased TSP-1 expression at the mRNA and protein levels, by controlling the TSP-1 promoter activity. Both TSA and exogenous TSP-1 reduced cell migration and capillary-like tube formation and these activities were confirmed by blocking TSP-1 with its neutralizing antibody and small-interfering RNA. Our results suggest that TSP-1 is a potent mediator of TSA-induced anti- angiogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiogenesis Inhibitors / pharmacology*
  • Animals
  • Cattle
  • Cell Line
  • Cell Movement / drug effects*
  • Endothelial Cells / drug effects
  • Endothelial Cells / physiology*
  • Humans
  • Hydroxamic Acids / pharmacology*
  • Neovascularization, Pathologic / metabolism
  • Neovascularization, Pathologic / prevention & control
  • Neovascularization, Physiologic / drug effects*
  • RNA, Messenger / biosynthesis
  • RNA, Small Interfering / genetics*
  • Thrombospondin 1 / biosynthesis*
  • Thrombospondin 1 / genetics
  • Thrombospondin 1 / pharmacology

Substances

  • Angiogenesis Inhibitors
  • Hydroxamic Acids
  • RNA, Messenger
  • RNA, Small Interfering
  • Thrombospondin 1
  • trichostatin A