Abstract |
Triflavin, an Arg-Gly-Asp (RGD) containing peptide purified from Trimeresurus flavoviridis snake venom, inhibits human platelet aggregation by blocking fibrinogen binding to fibrinogen receptors associated with glycoprotein IIb/IIIa complex. In this study, we show that triflavin (1-30 micrograms/mouse) inhibits B16-F10 melanoma cell-induced lung colonization in C57BL/6 mice in a dose-dependent manner. In vitro, triflavin dose-dependently inhibits adhesion of B16-F10 melanoma cells to extracellular matrices (ECMs; i.e., fibronectin, fibrinogen, vitronectin, and collagen type I). Triflavin is approximately 600-800 times more potent than GRGDS at inhibiting cell adhesion. In addition, triflavin dose-dependently inhibits B16-F10 cell-induced platelet aggregation. These results imply that the inhibitory effect of triflavin on the adhesion of tumor cells to ECMs (e.g., fibronectin, vitronectin and collagen type I) and/or tumor cell-induced platelet aggregation may be partially responsible for its antimetastatic activity in C57BL/6 mice.
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Authors | J R Sheu, C H Lin, J L Chung, C M Teng, T F Huang |
Journal | Japanese journal of cancer research : Gann
(Jpn J Cancer Res)
Vol. 83
Issue 8
Pg. 885-93
(Aug 1992)
ISSN: 0910-5050 [Print] Japan |
PMID | 1399825
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents
- Crotalid Venoms
- Peptides
- Platelet Aggregation Inhibitors
- triflavin
- Thymidine
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Topics |
- Animals
- Antineoplastic Agents
(pharmacology)
- Cell Adhesion
(drug effects)
- Cell Survival
(drug effects)
- Crotalid Venoms
(pharmacology)
- DNA Replication
(drug effects)
- Kinetics
- Lung Neoplasms
(prevention & control, secondary)
- Melanoma, Experimental
(blood, pathology, prevention & control)
- Mice
- Mice, Inbred C57BL
- Peptides
(pharmacology)
- Platelet Aggregation
(drug effects)
- Platelet Aggregation Inhibitors
(pharmacology)
- Thymidine
(metabolism)
- Tumor Cells, Cultured
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