Trichostatin A, an inhibitor of histone deacetylase, inhibits hypoxia-induced angiogenesis

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Abstract
Trichostatin A (TSA), a hydroxamate-type inhibitor of mammalian histone deacetylases has been reported to inhibit angiogenesis both in vitro and in vivo. TSA inhibits hypoxia-induced production of the angiogenic mediator vascular endothelial cell growth factor (VEGF) by tumour cells and also inhibits directly endothelial cell migration and proliferation. HDAC inhibitors such as TSA are currently of major interest as potential anticancer therapeutics, largely because of their well documented properties of inhibiting proliferation and inducing apoptosis of tumour cells. The finding that HDAC appears to be a critical regulator of angiogenesis in addition to tumour cell growth will heighten interest in the development of HDAC inhibitors as potential anticancer drugs.