Fig. 7
DS18561882 inhibits CRPC progression in vitro and in vivo. A-B. Cell proliferation and cell apoptosis assays of LNCaP cells transfected with empty vector or PPFIA4 overexpression plasmid (A) and C4-2B cells transfected with siNC or siPPFIA4 (B) with or without DS18561882 (50μM) treatment. **p < 0.01, ***p < 0.001. d, days. C-E. Castrated mice possessing xenografts (LNCaP-Vector and LNCaP-PPFIA4) received vehicle control or DS18561882 treatment (100 mg/kg, n = 5/group, p.o.). Caliper measurements were taken twice every week to obtain tumor volume (C). Tumors were collected and weighed (D) after the mice were sacrificed. IHC staining of Ki67 (E) on tumor slide from each group is shown. **p < 0.01, ***p < 0.001. Scale bars, 20 μm. p.o., peros. F-G. Cell proliferation (F) and cell apoptosis assays (G) of C4-2B (left) and LNCaP cells (right) treated with DMSO, enzalutamide (10 μM), DS18561882 (50 μM) alone or in combination. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. d, days. ENZ, enzalutamide. COM, combination. H-J. Castrated mice bearing xenografts (C4-2B cells) were treated with vehicle control, enzalutamide (10 mg/kg, p.o.), DS18561882 (100 mg/kg, p.o.), or in combination (n = 5/group). Tumor volume was measured (H) and then weighed (I) when mice were sacrificed. IHC staining of Ki67 (J) on tumor slides from each group is shown. ***p < 0.001, ****p < 0.0001. Scale bars, 20 μm. p.o., peros. ENZ, enzalutamide. COM, combination