Anthraquinone derivative emodin inhibits tumor-associated angiogenesis through inhibition of extracellular signal-regulated kinase 1/2 phosphorylation

被引：53

作者：

Kaneshiro, Tatsuya ^{[1
]}

Morioka, Takamitsu ^{[1
]}

Inamine, Morihiko ^{[1
]}

Kinjo, Tatsuya ^{[1
]}

Arakaki, Junya ^{[1
]}

Chiba, Itaru ^{[1
]}

Sunagawa, Nao ^{[1
]}

Suzui, Masumi ^{[1
]}

Yoshimi, Naoki ^{[1
]}

机构：

[1] Univ Ryukyus, Fac Med, Okinawa 9030215, Japan

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2006年 / 553卷 / 1-3期

关键词：

emodin; angiogenesis; human umbilical cord vein endothelial cells; ERK; 1/2;

D O I：

10.1016/j.ejphar.2006.09.026

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

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.

引用

页码：46 / 53

页数：8

共 38 条

[1] Tumorigenicity depends on angiogenic potential of tumor cells: Dominant role of vascular endothelial growth factor and/or fibroblast growth factors produced by tumor cells [J].