Interferon stimulates cholesterol and phosphatidylcholine synthesis but inhibits cholesterol ester synthesis in HeLa-S3 cells.

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Abstract
Treatment of human HeLa-S3 cells (an epidermoid carcinoma line) with human .beta.-interferon (640 units/ml) selectively alters lipid metabolism by increasing cholesterol synthesis per mg of cell protein as measured by 1-h pulse-labeling of cells with [3H]acetate. Cholesterol synthesis in interferon-treated cells is increased .apprxeq. 60% at 24 h after the beginning of treatment and .apprxeq. 450% at 48 h. Continuous labeling of interferon-treated cells with [14C]acetate shows increased accumulation of label in cholesterol when normalized per mg of cell protein, as well as an increase in the specific activity of cholesterol in the treated cells. Interferon treatment decreases the accumulation of [14C]acetate into cholesterol esters. The [14C]acetate labeling of sphingomyelin, phosphatidylethanolamine and triglycerides shows no change compared to untreated controls. The labeling of phosphatidylcholine was moderately increased in treated cells. The interferon-induced changes in lipid metabolism are a part of a coordinated response of cells to interferon treatment, characterized by reduced cell proliferation and cell motility and an increase in cell size and mass. The increased cholesterol synthesis is consistent with a model in which .beta.-interferon treatment of HeLa cells inhibits the endocytosis of cholesterol-containing low density lipoprotein, which results in an increase in cholesterol synthesis.