Ethyl pyruvate, an anti-inflammatory agent, inhibits tumor angiogenesis through inhibition of the NF-κB signaling pathway

• Published in: Cancer letters 2011-04, Vol.303 (2), p.150-154
• Main Authors: Park, Shi-Young, Yi, Eui-Yeun, Jung, Myunghwan, Lee, You Mie, Kim, Yung-Jin
• Format: Article
• Language: English
• Subjects: Administration, Oral; Angiogenesis; Angiogenesis Inhibitors - pharmacology; Animals; anti-inflammatory activity; anti-inflammatory agents; Anti-Inflammatory Agents - pharmacology; Anti-tumor; Carcinoma, Lewis Lung - metabolism; cell growth; Cell Line, Tumor; Cell Movement; Collagen - chemistry; Drug Combinations; endothelial cells; Endothelial Cells - cytology; Ethyl pyruvate; Hematology, Oncology and Palliative Medicine; Humans; Laminin - chemistry; lung neoplasms; Mice; Mice, Inbred C57BL; Neovascularization, Pathologic; NF-kappa B - metabolism; NF-κB; Proteoglycans - chemistry; Pyruvates - pharmacology; pyruvic acid; Signal Transduction; therapeutics; Vascular Endothelial Growth Factor A - metabolism; Wound Healing
• ISSN: 0304-3835; 1872-7980
• DOI: 10.1016/j.canlet.2010.12.024

Abstract Ethyl pyruvate (EP), simple derivative of pyruvate, has been shown to have anti-inflammatory properties. Here, we demonstrate EP’s strong anti-angiogenic activity. EP inhibited in vivo angiogenesis in the mouse Matrigel-plug assay and tumor growth in the mouse Lewis lung carcinoma model. EP also interfered with the angiogenic cascade, including growth, invasion, migration, and tube formation. Activation of NF-κB by vascular endothelial cell growth factor was reduced by EP. Taken together, we suggest that EP may have potential as a new multi-functional drug candidate for anti-angiogenesis and cancer therapy.