Inhibition of hypoxia-induced angiogenesis by sodium butyrate, a histone deacetylase inhibitor, through hypoxia-inducible factor-1α suppression

  • Authors:
    • Se-Hee Kim
    • Kyu-Won Kim
    • Joo-Won Jeong
  • View Affiliations

  • Published online on: April 1, 2007     https://doi.org/10.3892/or.17.4.793
  • Pages: 793-797
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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-1α in HT1080 human fibrosarcoma cells. Moreover, sodium butyrate also suppressed the hypoxia-stimulated angiogenic effects and downregulated HIF-1α 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-1α mediated angiogenesis under hypoxic conditions.

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April 2007
Volume 17 Issue 4

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Copy and paste a formatted citation
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Spandidos Publications style
Kim S, Kim K and Jeong J: Inhibition of hypoxia-induced angiogenesis by sodium butyrate, a histone deacetylase inhibitor, through hypoxia-inducible factor-1α suppression. Oncol Rep 17: 793-797, 2007
APA
Kim, S., Kim, K., & Jeong, J. (2007). Inhibition of hypoxia-induced angiogenesis by sodium butyrate, a histone deacetylase inhibitor, through hypoxia-inducible factor-1α suppression. Oncology Reports, 17, 793-797. https://doi.org/10.3892/or.17.4.793
MLA
Kim, S., Kim, K., Jeong, J."Inhibition of hypoxia-induced angiogenesis by sodium butyrate, a histone deacetylase inhibitor, through hypoxia-inducible factor-1α suppression". Oncology Reports 17.4 (2007): 793-797.
Chicago
Kim, S., Kim, K., Jeong, J."Inhibition of hypoxia-induced angiogenesis by sodium butyrate, a histone deacetylase inhibitor, through hypoxia-inducible factor-1α suppression". Oncology Reports 17, no. 4 (2007): 793-797. https://doi.org/10.3892/or.17.4.793