2006年12月
Anthraquinone derivative emodin inhibits tumor-associated angiogenesis through inhibition of extracellular signal-regulated kinase 1/2 phosphorylation
EUROPEAN JOURNAL OF PHARMACOLOGY
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- 巻
- 553
- 号
- 1-3
- 開始ページ
- 46
- 終了ページ
- 53
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/j.ejphar.2006.09.026
- 出版者・発行元
- ELSEVIER SCIENCE BV
An anthraquinone derivative, emodin, suppresses tumor development both in vitro and in vivo. in this study, we examined the anti-angiogenic activity of emodin and its modifying effect on the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2. In cell cultures, emodin inhibited endothelial cell proliferation, migration, and tube formation in a dose-dependent manner. In addition, the mouse dorsal air sac assay revealed the vivo anti-angiogenic potential of emodin. Matrix metalloproteinase-9 (MMP-9) expression, which is critical for the angiogenic process, including migration and tube formation, decreased after exposure to emodin, as determined by polymerase chain reaction with reverse transcription (RT-PCR) and gelatin zymography. Moreover, the phosphorylation of ERK 1/2 decreased after exposure to emodin in a dose-dependent manner. These observations suggest that emodin has the potential to inhibit several angiogenic processes and that these effects may be related to suppression of the phosphorylation of ERK 1/2. (c) 2006 Elsevier B.V. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/j.ejphar.2006.09.026
- ISSN : 0014-2999
- Web of Science ID : WOS:000242772600006