Abstract
The role of fibrinogen covalently associated with cell membrane in blood-borne lung tumor colony formation of murine mammary carcinoma cells in mice was studied. When mice were treated with prednisolone, their plasma fibrinogen levels profoundly increased. Hyperfibrinogenemia, induced by prednisolone treatment or plasma fibrinogen infusion of syngeneic mice, accelerated the coagulation time and significantly increased the number of lung tumor colonies of SCK tumor cells. Hypofibrinogenemia, induced by rabbit antisyngenic mouse fibrinogen immunoglobulin G or heparin infusion, markedly delayed coagulation time and prominently reduced the numbers of blood-borne lung tumor colonies of the tumor cells. SCK mammary carcinoma cells form a coating of fibrinogen on their surfaces in a medium containing fibrinogen. This coating is cross-linked in a manner characteristic of catalysis by tumor cell membrane-bound transglutaminase K. The fibrinogen coating on the surface of these tumor cells functions to protect against autologous lymphokine-activated killer cells. These results provide information on the impact of fibrin stability on blood-borne lung tumor colony formation of SCK mammary carcinoma cells.
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