Triflavin, an Arg‐Gly‐Asp‐containing Antiplatelet Peptide Inhibits Cell‐substratum Adhesion and Melanoma Cell‐induced Lung Colonization

• Published in: Cancer science 1992-08, Vol.83 (8), p.885-893
• Main Authors: Sheu, Joen R., Lin, Chao H., Chung, Jih L., Teng, Che M., Huang, Tur F.
• Format: Article
• Language: English
• Subjects: Animal tumors. Experimental tumors; Animals; Antineoplastic Agents - pharmacology; Biological and medical sciences; Cell adhesion; Cell adhesion & migration; Cell Adhesion - drug effects; Cell Survival - drug effects; Collagen (type I); Colonization; Crotalid Venoms - pharmacology; DNA Replication - drug effects; Experimental respiratory system tumors; Extracellular matrix; Fibrinogen; Fibronectin; Key words; Kinetics; Lung Neoplasms - prevention & control; Lung Neoplasms - secondary; Medical sciences; Melanoma; Melanoma, Experimental - blood; Melanoma, Experimental - pathology; Melanoma, Experimental - prevention & control; Mice; Mice, Inbred C57BL; Peptides; Peptides - pharmacology; Platelet aggregation; Platelet Aggregation - drug effects; Platelet Aggregation Inhibitors - pharmacology; RGD‐containing peptide; Thymidine - metabolism; Tumor cell metastasis; Tumor cells; Tumor Cells, Cultured; Tumors; Venom; Vitronectin
• ISSN: 0910-5050; 1347-9032; 1349-7006; 1876-4673
• DOI: 10.1111/j.1349-7006.1992.tb01995.x

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 Ilb/IIIa complex. In this study, we show that triflavin (1‐30 μg/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.