Abstract
Hypoxia-inducible factor-1 (HIF-1) plays a pivotal role in cellular response to low oxygen concentration, such as angiogenesis in tumors. Here, we found that a histone deacetylase inhibitor, sodium butyrate, inhibits the hypoxia-induced induction and activity of HIF-1alpha in HT1080 human fibrosarcoma cells. Moreover, sodium butyrate also suppressed the hypoxia-stimulated angiogenic effects and downregulated HIF-1alpha and vascular endothelial growth factor expression in vascular endothelial cells. These findings suggest that sodium butyrate may play important roles in tumor suppression via inhibition of HIF-1alpha mediated angiogenesis under hypoxic conditions.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Angiogenesis Inhibitors / pharmacology*
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Aryl Hydrocarbon Receptor Nuclear Translocator / antagonists & inhibitors*
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Aryl Hydrocarbon Receptor Nuclear Translocator / metabolism
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Butyrates / pharmacology*
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Down-Regulation
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Gene Expression
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Histone Deacetylase Inhibitors*
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Humans
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Hypoxia / metabolism
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Neoplasms / blood supply*
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Neovascularization, Pathologic / metabolism*
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Sodium / pharmacology
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Vascular Endothelial Growth Factor A / genetics
Substances
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Angiogenesis Inhibitors
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Butyrates
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Histone Deacetylase Inhibitors
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Vascular Endothelial Growth Factor A
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Aryl Hydrocarbon Receptor Nuclear Translocator
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Sodium