Fig. 3: CRYAB is the candidate to mediate its tumor-suppressive activity in PCa.

a Workflow of the candidate screening. b Correlation analysis between MITF and CRYAB expression in primary tumor (PT) specimens of different PCa datasets. Sample sizes: Taylor, n = 131; Grasso, n = 49; Lapointe, n = 13; TCGA provisional data, n = 495; and Glinsky, n = 78. c CRYAB expression in normal prostate and primary tumor (PT) specimens in different PCa datasets^{9,10,11,12,13}. Sample sizes: Taylor (N, n = 29; PT, n = 130); Grasso (N, n = 12; PT, n = 49); Varambally (N, n = 6; PT, n = 7); Lapointe et al. (N, n = 9; PT, n = 13), and Tomlins (N, n = 22; PT, n = 32). Data from Taylor dataset correspond to the mean signal of all isoforms of the transcripts. In (b) and (c), each dot corresponds to an individual specimen. d Western blot analysis of CRYAB expression in benign prostatic hyperplasia (BPH) and PCa specimens from Basurto University Hospital cohort (BPH n = 7 patient specimens; PCa n = 14 patient specimens). e Chromatin immunoprecipitation (ChIP) of exogenous MITF on CRYAB promoter in PC3 TRIPZ-MITFA cells after induction with 0.5 µg mL⁻¹ doxycycline for 3 days (n = 4–5). Binding to ANGPT4 was used as a negative control. Final data were normalized to IgG (negative-immunoprecipitation control) and to No dox condition. No dox: MITFA noninduced conditions; Dox: MITFA-induced conditions. Statistic tests: Spearman correlation (b); Mann−Whitney test (c); one-sample t test (e); Error bars represent s.e.m. *p < 0.05, **p < 0.01