dinoprost and Facial-Neoplasms

We studied the response of a human squamous cell carcinoma cell line, SCC-12F, to human complement attack and found that the cells were completely resistant to complement lysis. In the absence of lysis, there was significant C3 deposition and C5b-9 deposition on the cells. Removal of the lipid-linked complement regulatory proteins CD59 and decay-accelerating factor (DAF) by treatment of the cells with phosphatidylinositol-specific phospholipase C (PIPLC) resulted in increased C3b and C5b-9 deposition on the cells and a slight increase in cell death. Treatment of the cells with complement caused them to release membrane vesicles containing the terminal complement proteins. In addition, complement induced SCC-12F to produce significant amounts of prostaglandin F2alpha (PGF2alpha). We conclude that CD59 and DAF are important in the resistance of SCC-12F to complement and that these cells produce membrane vesicles and PGF2alpha in response to complement attack. These responses, in the absence of cell death, may be important in the pathogenesis of inflammatory skin disease in which complement is deposited.

Topics: Animals; Carcinoma, Squamous Cell; Complement Inactivator Proteins; Complement Membrane Attack Complex; Complement System Proteins; Cytotoxicity, Immunologic; Dinoprost; Facial Neoplasms; Humans; Immune Sera; Keratinocytes; Phosphatidylinositol Diacylglycerol-Lyase; Phosphoinositide Phospholipase C; Rabbits; Skin Neoplasms; Tumor Cells, Cultured; Type C Phospholipases