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Sex Hormone-Binding Globulin Secretion by Human Hepatocarcinoma Cells Is Increased by Both Estrogens and Androgens^*

School of Medical Technology, Western Australian Institute of Technology Bentley, Western Australia 6102
University Department of Obstetrics and Gynecology, University of Western Australia Western Australia 6009

Address requests for reprints and all correspondence to: Dr. I. R. Lee, School of Medical Technology, Western Australian Institute of Technology, Kent Street, Bentley, Western Australia 6102.

The secretion of sex hormone-binding globulin (SHBG) by the human hepatocarcinoma cell line Hep G2 was increased significantly not only by estradiol (E₂) but also by testosterone (T), dihydrotestosterone, and the synthetic andro-gen danazbl in the presence, but not the absence, of fetal calf serum. The secretion of SHBG also was stimulated by the antiestfogen tamoxifen, although this required the use of longer incubation periods and higher concentrations than were required for the steroids. The antiandrogen cyproterone acetate and cortisol (5 µM) decreased SHBG secretion. Pregnanediol (5 µM) had no discernible effect. These changes were considered specific as none of the compounds altered either the secretion of total protein by the cells or their total protein content. Cells incubated with a mixture of E₂ (0.5 µM) and T (0.5 µM) secreted significantly more SHBG than did cells incubated with E₂ (1.0 µM), indicating these steroids exert their effects through different mechanisms. The increases with E₂ and T were reduced significantly by tamoxifen and cyproterone acetate, respectively, suggesting receptor mediation of the steroid effects. The E₂-related increase was abolished by cycloheximide, indicating that the changes were due to alterations in the synthesis of SHBG rather than to alterations in the release of previously synthesized protein. These findings suggest the T-related decrease in plasma SHBG levels may be due to causes other than a decrease in the hepatic synthesis of the protein. Additionally, they indicate that Hep G2 cells may prove suitable for examining the regulation of the SHBG gene by a variety of compounds.

^* This study was supported by grants from the Cancer Foundation of Western Australia and the Western Australian Institute of Technology.

Received August 14, 1986.

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