V Fulop1, M A Steller, R S Berkowitz, D J Anderson. 1. Fearing Research Laboratory, Harvard Medical School, Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Boston, MA 02115.
Abstract
OBJECTIVES: This study was performed to further define the effects of interferon-gamma on choriocarcinoma cell lines and to determine whether variations in response among cell lines are attributable to quantitative differences in interferon-gamma receptors. STUDY DESIGN: Interferon-gamma receptors were quantified on BeWo, JEG-3 and Jar choriocarcinoma cell lines by a radiolabeled interferon-gamma ligand binding assay. The response of these cell lines to interferon-gamma was measured in two functional assays: a cell proliferation assay and a cell lysis assay after exposure to interferon-gamma with and without actinomycin-D. RESULTS: The number of interferon-gamma receptors on BeWo, Jar, and JEG-3 cells did not differ significantly (650, 560, and 420 interferon-gamma receptors per cell, respectively). Proliferation of all three choriocarcinoma cell lines was significantly inhibited to a similar extent by interferon-gamma. After treatment with interferon-gamma actinomycin-D, each choriocarcinoma cell line exhibited dose-dependent cell lysis; lysis of Jar was significantly less than that of either BeWo or JEG-3. CONCLUSION: These data further document variations in the response of choriocarcinoma cell lines to interferon-gamma and indicate that these differences are not the result of interferon-gamma receptor number but of postreceptor mechanisms.
OBJECTIVES: This study was performed to further define the effects of interferon-gamma on choriocarcinoma cell lines and to determine whether variations in response among cell lines are attributable to quantitative differences in interferon-gamma receptors. STUDY DESIGN:Interferon-gamma receptors were quantified on BeWo, JEG-3 and Jar choriocarcinoma cell lines by a radiolabeled interferon-gamma ligand binding assay. The response of these cell lines to interferon-gamma was measured in two functional assays: a cell proliferation assay and a cell lysis assay after exposure to interferon-gamma with and without actinomycin-D. RESULTS: The number of interferon-gamma receptors on BeWo, Jar, and JEG-3 cells did not differ significantly (650, 560, and 420 interferon-gamma receptors per cell, respectively). Proliferation of all three choriocarcinoma cell lines was significantly inhibited to a similar extent by interferon-gamma. After treatment with interferon-gammaactinomycin-D, each choriocarcinoma cell line exhibited dose-dependent cell lysis; lysis of Jar was significantly less than that of either BeWo or JEG-3. CONCLUSION: These data further document variations in the response of choriocarcinoma cell lines to interferon-gamma and indicate that these differences are not the result of interferon-gamma receptor number but of postreceptor mechanisms.