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. 2021 Feb 15;131(4):e141335. doi: 10.1172/JCI141335

Figure 7. CPPI inhibited LNCaP95 cell proliferation and full-length AR interaction with ARv7.

Figure 7

(A) LNCaP95 cell proliferation following treatment with indicated concentrations of CPPI for 1, 2, and 3 days (n = 3). (B) BrdU incorporation in LNCaP95 cells treated with CPPI. Right panel shows percentages of the LNCaP95 cells stained with BrdU (n = 4). Original magnification, ×40. (C) Cell-cycle analysis of LNCaP95 cells treated with CPPI (n = 3). (D) Western blot of AR, AR S81, PSA, and UBE2C in LNCaP95 cells treated with CPPI. GAPDH was probed as loading control. (E) qPCR analysis of AR target genes (KLK3, TMPRSS2, and NKX3-1) and ARV target genes (UBE2C and CDC20) in LNCaP95 cells treated with CPPI (n = 3). (F) Western blot analysis of AR and ARv7 in the nuclear and cytoplasmic extracts of LNCaP95 cells treated with CPPI. (G) BRET assay of AR-FL and ARv7 interaction following CPPI treatment (n = 3). Quantitative data are presented as mean ± SEM, and all data represent 1 of at least 2 independent experiments with consistent results. Unpaired t test (A) or 1-way ANOVA with Dunnett’s multiple-comparison post test (B, C, E, and G) was used to determine statistical significance. *P < 0.05; **P < 0.01; ***P < 0.001.