Fig. 6: SRGs are prognostic and associated with splicing dysregulation.

a Kaplan–Meier plots for representative unfavorable and favorable genes associated with patient overall survival in seven different cohorts. b Numbers of genes showing favorable and unfavorable prognostic effects in five distinct cohorts. Patient numbers for each cohort are shown in parentheses. c Meta-analysis showing a higher level of unfavorable signature (13 genes: SRSF1, KHDRBS3, ESRP1, HNRNPH1, U2SURP, LSM5, TIA1, CHERP, HNRNPR, HNRNPH2, HNRNPH3, HNRNPAB, and KHDRBS1, with each showing consistent unfavorable prognosis in ≥3 datasets) and a lower level of favorable signature (13 genes: MFAP1, SF3A2, GPATCH1, XAB2, CELF2, SF3A1, SAP18, SRP54, PPIL2, SF1, MATR3, ELAVL4, and CDK10 with each showing consistent favorable prognosis in ≥2 datasets) correlating with reduced overall patient survival, respectively. Data were based on the Setlur and Glinsky studies. d, e Unfavorable signature is associated with higher Gleason score (d) and a higher level of unfavorable signature positively correlates with disease recurrence in TCGA cohort (e). In d, the center white dots represent median values, box edges are 75th and 25th percentiles, and whiskers denote the maximum and minimum values, respectively. Shown in e is biochemistry recurrence (BCR)-free survival. f DSEs associated with high or low expression level of unfavorable signature in primary PCa cohort. The p-value was calculated using two-tailed unpaired Student’s t-test (d) and log-rank test (a, c, e). See Supplementary Data 5 for details.