Fig. 8
From: Drugging the intrinsically disordered transactivation domain of androgen receptor
Potential of ARTADIs as a treatment for eugonadal prostate cancer patients. a Full-length AR (~110 kDa) and AR-V (~75 kDa) protein levels in androgen-stimulated cells treated with inhibitors. β-actin was used as a loading control. A representative blot is provided from n = 3–5 independent experiments. b Left panel - temporal tumor growth of subcutaneous LNCaP xenografts in NSG mice that were all castrated (Cx) and then supplemented with a time-release testosterone (T) pellet. Daily gavage treatments of vehicle with no T-pellet (VEH Cx); vehicle plus T-pellet (VEH + T); enzalutamide plus T-pellet (ENZA + T); and BU170 plus T-pellet (BU170 + T). Middle panel shows the final tumor volumes at day 16. Right panel shows final body weight changes for each mouse. c Transcript levels of AR and androgen-regulated genes, and d cell cycle genes that were normalized to the housekeeping gene SDHA using RNA isolated from xenografts shown in b. Data is normalized to VEH + T control and presented as mean ± SEM, and analyzed by one-way ANOVA with Dunnet’s correction. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. See Supplementary Fig. 7b, c
