The Wedelolactone Derivative Inhibits Estrogen Receptor-Mediated Breast, Endometrial, and Ovarian Cancer Cells Growth
Figure 1
BTB selectively inhibits E2-mediated ER transactivation, moderately inhibits DHT-mediated AR transactivation, and fails to inhibit the PR and GR activity. (a) Chemical structures of wedelolactone and BTB. (b) and (c) BTB at 2.5, 5.0, and 10 μM concentrations can effectively inhibit the estrogen-induced ERα or ERβ transcriptional activity in HEK293 cells. (d) BTB moderately inhibits the androgen-induced AR transcriptional activity in HEK 293 cells. BTB at 5.0 μM concentration could not inhibit the AR transactivation, and 10 μM of BTB treatment started to show about 15–20% inhibition of the AR transactivation. (e)–(g) Inhibition of BTB on the E2-induced ER transcriptional activity in MCF-7, Ishikawa, and SKOV-3 cells. (h) and (i) Noeffects of BTB on the transcriptional activities of P4-induced PR and Dex-induced GR in Ishikawa cells. MMTV-Luc was used to determine the AR, PR, and GR mediated transactivation. ERE-Luc was used to assay ERα and ERβ mediated transactivation activities. Data represent mean ± SD collected from three independent experiments with duplication in each experiment.
