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  • Title: Mode of estrogen action on cell proliferation in CAMA-1 cells: III. Effect of antiestrogen.
    Author: Leung BS.
    Journal: Anticancer Res; 1987; 7(2):219-25. PubMed ID: 3592635.
    Abstract:
    Estrogen (E) stimulatory effects on mammary carcinoma are well documented; however, little is known of the precise mechanism regulating E-induced cell proliferation. This study attempts to investigate the in vitro effects of E and antiestrogen (AE) on promoting cell proliferation and the cell cycle kinetics of an experimental mammary carcinoma model, CAMA-1. Sublines IR and IN, which have been shown to respond to E somewhat differently in 3H-thymidine (3H-dThd) uptake and in the induction of progesterone receptor (Cancer Res 41: 5004-5009, 1981), were evaluated concurrently. The present report showed that E stimulated and AE, as shown by tamoxifen (TAM) and nafoxidine hydrochloride (NAF), inhibited cell growth and 3H-dThd uptake in a dose-related manner for both sublines supplemented with serum. In a chemically defined medium with 1% steroid-stripped serum, the E-stimulatory effect was nullified, and cells were more sensitive to AE. These results suggest that serum component(s) is (are) involved in AE and E action. The TAM inhibition could be partially reversed by E. A partially synchronized G1 population, arrested by serum deprivation for 48 hrs, responded promptly to E stimulation. While E promoted a faster G1 exit, faster for IN cells than for IR subline, AE inhibited cell progression at the G1 phase. Furthermore, E stimulated a higher proportion of S-phase formation during the first cycle of hormone treatment while AE inhibited this process. These results are consistent with the notion that TAM and E act on some common events at the G1 phase in cell proliferation. The net result of E stimulation was the promotion of new cell to traverse the cell cycle, the acceleration of G1 exit, and an increase in the proportion of S-phase and dividing cells per cycle. In contrast, AE inhibited the progression of cells at the G1 phase, resulting in a marked decrease of S-phase and dividing cells per cycle. Our results also demonstrate the importance of careful kinetic studies in evaluating the E and AE responses of mammary carcinoma cells in culture, and this is best conducted with synchronized populations.
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