Fig. 3.

AR, PR, and ER are functional, regulate endogenous genes and growth of BCK4 cells. a Transcription assays were performed with exogenous reporter constructs containing progesterone response elements (PRE₂) or estrogen response elements (ERE₂) as described. Cells were treated with vehicle (open bars) or hormone (solid bars) with the progestins R5020 or MPA, the glucocorticoid dexamethasone (DEX), the androgen R1881, or estradiol (E2). b Semi-quantitative PCR of BCK4 cells treated with vehicle (Et; EtOH) progestin (R5; R5020), androgen (R18; R1881), and glucocorticoid (Dex; Dexamethasone). Responsive genes were assayed at two different timepoints of hormone treatment, 6 or 24 h. Two different doses of Dex were used, 100 and 1,000 nM. GAPDH was used as an internal control. Semi-quantitative PCR analysis of BCK4 cells treated with vehicle (Et; EtOH) or estrogen (E2) for 6 or 24 h. Two estrogen responsive genes, pS2 and CathD were measured. GAPDH was used as a loading control. c MTS cell proliferation assay of BCK4 cells treated with vehicle (EtOH), estradiol (E2), androgen (R1881), progestin (R5020), or the progestin/androgen (MPA). Cells were assayed at 0, 72, 144, and 192 h of treatment