MECR-associated metabolic regulation contributes to tumor progression and immune microenvironment remodeling in prostate cancer

Prostate cancer is a worldwide leading malignancy, and the exploration of initiation mechanisms and therapeutic targets remains an important challenge. In this study, transcriptomic and clinical data from wide-used prostate cancer cohorts were integrated to establish a novel prognostic model and explore the biological significance of its core genes. Differential expression analysis combined with LASSO-Cox regression identified a three-gene prognostic model consisting of MECR, HVCN1, and NGFR. This model could independently predict patient outcomes and demonstrated superior predictive performance compared with conventional clinicopathological variables. Among these genes, MECR was the only one associated with poor prognosis. Functional studies revealed that MECR could promote proliferation, migration, and reduce apoptosis-related nuclear morphological changes in prostate cancer cell. Mechanistically, MECR could regulate PI3K/AKT pathway activity and immune-related cell mechanisms. In immunocompetent syngeneic tumor models, MECR knockdown significantly inhibited tumor progression and was associated with increased CD8 + T-cell activation. We found that CD8 + T-cell depletion could partially rescue the antitumor effects of MECR silencing, indicating that CD8 + T-cell-mediated immunity contributes to the antitumor effects of MECR silencing. Collectively, our findings identify MECR as a potential regulator linking tumor progression, apoptosis-related cellular phenotype, and immune microenvironment remodeling in prostate cancer. By integrating tumor-intrinsic and immune-associated mechanisms, our results provide new insights into molecular pathways in prostate cancer development and immune evasion related therapeutic resistance.