SRRT promotes prostate cancer progression and serves as a prognostic biomarker through STAT3 pathway activation

Prostate cancer (PC) is a highly prevalent malignancy in men with substantial prognostic heterogeneity. The present study aimed to identify novel prognostic biomarkers and investigate their functional roles and underlying mechanisms in PC. To this end, integrated bioinformatics analyses were performed using The Cancer Genome Atlas‑prostate adenocarcinoma cohort and two Gene Expression Omnibus datasets. A total of 95 common differentially expressed genes were identified and were significantly enriched in the STAT3 signaling pathway. Lasso and Cox regression analyses screened nine independent prognostic genes, among which SRRT exhibited the highest risk coefficient. The constructed risk model showed strong predictive performance for disease‑free survival and favorable calibration in nomogram analysis. Experimental validation demonstrated that SRRT was markedly upregulated in PC tissues and cell lines, and functional assays revealed that SRRT knockdown inhibited, whereas overexpression promoted, proliferation and migration of DU145 and PC‑3 cells in vitro and tumor growth in vivo. Mechanistically, SRRT enhanced STAT3 phosphorylation, and activation of STAT3 by colivelin partially reversed the suppressive effects of SRRT silencing, indicating that SRRT promotes PC progression through activation of the STAT3 signaling pathway. Collectively, SRRT acts as an independent adverse prognostic biomarker that promotes PC progression, and the present findings provide integrated bioinformatic and experimental evidence linking SRRT to STAT3 pathway activation.