The cGAS-STING pathway, as a key molecular mechanism within the innate immune system for recognizing cytoplasmic DNA, activates type I interferon and inflammatory cytokine responses upon sensing abnormal DNA originating from genomic, mitochondrial, or exogenous pathogens. This pathway subsequently participates in regulating multiple biological processes, including tumourigenesis, immune evasion, and therapeutic resistance. Prostate adenocarcinoma is a common malignant tumour in males, whose development is closely associated with genomic instability, dysregulation of the androgen receptor signaling pathway, and a local chronic inflammatory microenvironment. Recent studies have revealed that the cGAS-STING pathway exhibits dual roles in prostate adenocarcinoma: on one hand, it can initiate anti-tumour immune responses to inhibit tumour progression; on the other hand, it may also promote disease progression by inducing immune suppression or metabolic reprogramming. This paper provides a systematic review of the cGAS-STING pathway’s mechanisms of action in prostate adenocarcinoma, current research status, and its clinical translational prospects as a therapeutic target.
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