Fig. 5
WT SPOP promotes, while the prostate cancer-associated SPOP mutants inhibit stress-induced cell death. a The cell death analysis (PI staining) of C4–2 cells stably expressing EV, SPOP-WT, ΔNLS, F125 V, or F133 L treated with DMSO, AS (100 μM, 2 h), H2O2(2 h)or Docetaxel (DOC, 10 μM, 4 h) .b The tumor image of parental and Caprin1 knockout C4–2 cells implanted tumors from nude mice. c, d Weight (c) and growth curve (d) and of implanted tumors formed by parental and Caprin1 knockout C4–2 cells. n = 4. e The cell death analysis of parental and Caprin1 knockout C4–2 cells treated with DMSO, AS (100 μM, 2 h), H2O2 (2 h) or DOC (10 μM, 12 h). f The cell death analysis of C4–2 cells stably expressing EV, Caprin1-WT, or ΔSBC treated with DMSO, AS (100 μM, 2 h), H2O2(2 h)or DOC (10 μM, 12 h) . g Western blot of WCLs from C4–2 cells stably expressing EV, SPOP-WT, or SPOP-ΔNLS treated with DMSO, AS (100 μM, 2 h), H2O2(2 h)or DOC (10 μM, 12 h) . h Representative IHC images of Caprin1 staining in SPOP wild-type or mutant primary human prostate cancer samples. The scale bar: 400 μm or 100 μm. i Quantitative data for the Caprin1 protein staining in (g). Statistical significance was determined by Wilcoxon rank-sum test. j RT-qPCR assessment of Caprin1 mRNA expression in SPOP-WT and SPOP-MUT prostate tumors. Caprin1 mRNA expression level in each tumor specimen was normalized by the expression level of 18S rRNA (internal control) and exhibited as a value. of log10. P values were determined by Mann-Whitney test (two-sided). k Comparing Caprin1 mRNA expression between SPOP-WT and SPOP-MUT prostate tumors using TCGA RNA-seq data. Y-axis indicates the mean-centered gene expression level pre calculated from pan-cancer analysis. P values were determined by non-parametric Wilcoxon rank sum test (two sided)