This paper reviews how a cell‑signaling system called cGAS‑STING can both help and hurt the fight against cancers of the prostate, kidney, and bladder. It shows that turning this pathway on can boost immune attacks on tumors, but in some cases it also helps tumors grow or resist treatment. The study does not give any practical tips for using palmitoyl‑dipeptide‑6 or any other DIY health hacks.

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon (IFN) genes (STING) pathway emerges as a dual-functional role in urologic malignancies, exhibiting context-dependent tumor-suppressive and pro-tumorigenic activities. When this pathway is activated in urologic tumors, IFN transcription and CD8⁺ T cell infiltration are triggered, which has an anticancer effect. However, this pathway facilitates the development of prostate cancer through the up-regulation of regulatory B cells. STING palmitoylation triggers immune escape in renal cell carcinoma, and the STING/SLC14A1 axis also mediates chemoresistance in bladder cancer. Based on these findings, we establish the first systematic comparison of tissue-specific STING regulation in urological malignancies, challenging the conventional tumor suppressor-centric view. This review also highlights several innovative strategies leveraging this duality during urologic cancers. The demand for the long-term safety and effectiveness of these targeted STING treatments has not been fully met. This study introduces a framework that harnesses the dual functions of the cGAS-STING pathway to strengthen immunotherapy approaches and improve clinical outcomes to bridge the pre-clinical-clinical gap. The context-dependent duality of cGAS-STING signalling in urologic tumours is revealed. Targeting the STING pathway, in combination with immunotherapies and gene therapies, enhances the anti-tumour response. Sex hormone differences in urological malignancies are correlated with the cGAS-STING pathway.