MOESM3 of Histone variant MacroH2A1 is downregulated in prostate cancer and influences malignant cell phenotype

Additional file 3: Fig. S1. Scatter blots representation of transcript levels of MacroH2A1.1 and QKI in matched PIN and PCa lesions from the same patients, assessed by RT-qPCR and normalized to GUSB mRNA levels. Fig. S2. Correlation between MacroH2A1 and H2A.Z transcript levels in prostate cancer samples, assessed by RT-qPCR and normalized to GUSB. Fig. S3. Scatter blots representation of distribution of MacroH2A1.1 mRNA levels in prostate cancer tissue samples, assessed by RT-qPCR and normalized to GUSB, according to categorized ≤ 10 ng/mL and > 10 ng/mL PSA levels. Fig. S4. Scatter blots representation of distribution of MacroH2A1.1 and QKI mRNA levels assessed by RT-qPCR and normalized to GUSB, among Gleason scores ≤ 6, 7 (3 + 4), 7 (4 + 3) and ≥ 8 prostate cancer tissue samples. Fig. S5. (a) Distribution of transcript levels of total MacroH2A1, MacroH2A1.1 and MacroH2A1.2, assessed by RT-qPCR and normalized to GUSB mRNA levels, in androgen-receptor positive prostate cancer cell lines (22Rv1, LNCaP and VCaP), and in androgen-receptor negative prostate cancer cell lines (DU145 and PC-3). (b) Distribution of transcript levels of splicing regulators DDX5, DDX17 and QKI, assessed by RT-qPCR and normalized to GUSB, in androgen positive and negative prostate cancer cell lines. (c) Distribution of MacroH2A1.1 and MacroH2A1.2 protein levels, normalized to β-actin, in androgen positive and negative prostate cancer cell lines. Mann–Whitney U-test: **p < 0.01, ***p < 0.001. ns—non significant