Abstract |
The growth and metastasis of tumors depend on angiogenesis. Tumor angiogenesis is initiated by the secretion of growth factors from tumor cells; downstream signals are then triggered in pre-existing blood vessels to sprout a new vascular network. Trichosanthin (TCS) is a type I ribosome-inactivating protein that has anti- tumor activity, but the underlying mechanism remains unclear. In this study, we found that a non-toxic dose of TCS decreased the wound-healing and the migration of H5V mouse heart capillary endothelial cells (ECs) induced by human choriocarcinoma (JAR) cells, as well as the JAR-induced angiogenesis of rat third-order mesenteric arteries. TCS was effective on both tumor cells and ECs/arteries. First, TCS decreased vascular endothelial growth factor transcription and secretion by JAR cells. Second, TCS consequently inhibited the tumor cell-induced, extracellular signal-regulated kinase-mediated angiogenic signal in ECs and blood vessels. In conclusion, the ability of TCS to inhibit tumor angiogenesis contributes to its anti- tumor activity.
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Authors | Dongxu He, Jian Jin, Yongtang Zheng, Iain C Bruce, Siucheung Tam, Xin Ma |
Journal | Biochemical and biophysical research communications
(Biochem Biophys Res Commun)
Vol. 430
Issue 2
Pg. 735-40
(Jan 11 2013)
ISSN: 1090-2104 [Electronic] United States |
PMID | 23206700
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2012 Elsevier Inc. All rights reserved. |
Chemical References |
- Angiogenesis Inhibitors
- Vascular Endothelial Growth Factor A
- Trichosanthin
- Extracellular Signal-Regulated MAP Kinases
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Topics |
- Angiogenesis Inhibitors
(pharmacology)
- Animals
- Cell Line, Tumor
- Cell Movement
(drug effects)
- Endothelial Cells
(drug effects, physiology)
- Extracellular Signal-Regulated MAP Kinases
(antagonists & inhibitors)
- Humans
- MAP Kinase Signaling System
(drug effects, physiology)
- Mice
- Neoplasms
(blood supply)
- Rats
- Trichosanthin
(pharmacology)
- Vascular Endothelial Growth Factor A
(physiology)
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