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Carcinogenesis Advance Access originally published online on February 18, 2009
Carcinogenesis 2009 30(4):655-661; doi:10.1093/carcin/bgp039
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Decursin and decursinol angelate inhibit VEGF-induced angiogenesis via suppression of the VEGFR-2-signaling pathway

Myung Hwan Jung, Sun Hee Lee, Eun-Mi Ahn1 and You Mie Lee*

Department of Natural Sciences, School of Life Sciences and Biotechnology, Kyungpook National University, Daegu 702-701, Republic of Korea
1 Department of Herbal Foodceutical Science, Daegu Haany University, Daegu 712-715, Republic of Korea

* To whom correspondence should be addressed. Tel: +82 53 950 7362; Fax: +82 53 943 6925; Email: lym{at}knu.ac.kr

Inhibition of angiogenesis is an attractive approach for the treatment of angiogenic diseases, such as cancer. Vascular endothelial growth factor (VEGF) is one of the most important activators of angiogenesis and interacts with the high-affinity tyrosine kinase receptors, VEGFR-1 and VEGFR-2. The pyranocoumarin compounds decursin and decursinol angelate isolated from the herb, Angelica gigas, are known to possess potent anti-inflammatory activities. However, little is known about their antiangiogenic activity or their underlying mechanisms. Here, we show the antiangiogenic effects of decursin and decursinol angelate using in vitro assays and in vivo animal experiments. Decursin and decursinol angelate inhibited VEGF-induced angiogenic processes in vitro, including proliferation, migration and tube formation of human umbilical vein endothelial cells. Decursin and decursinol angelate significantly suppressed neovessel formation in chick chorioallantoic membrane and tumor growth in a mouse model. The microvessel density in tumors treated with decursin for 14 days was significantly decreased compared with a vehicle control group. Decursin and decursinol angelate inhibited VEGF-induced phosphorylation of VEGFR-2, extracellular signal-regulated kinases and c-Jun N-terminal kinase mitogen-activated protein kinases. Taken together, these results demonstrate that decursin and decursinol angelate are novel candidates for inhibition of VEGF-induced angiogenesis.

Abbreviations: CAM, chorioallantoic membrane; ERK, extracellular signal-regulated kinase; GFP, green fluorescent protein; HUVEC, human umbilical vein endothelial cell; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; PMA, phorbol 12-myristate 13-acetate; VEGF, vascular endothelial growth factor

Received October 6, 2008; revised January 14, 2009; accepted January 29, 2009.


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