Key signaling pathways in the development and progression of prostate cancer: The crosstalk between inflammation, autophagy, and pyroptosis.

Prostate cancer is one of the most common malignant tumors of the male genitourinary system, with its incidence and mortality continuing to rise globally. This trend is particularly pronounced once the disease progresses to the castration-resistant stage, where current therapeutic options offer limited efficacy and drug resistance remains a major clinical challenge, severely compromising patient survival outcomes. Therefore, a systematic elucidation of the key biological mechanisms driving prostate cancer progression and therapeutic failure is of urgent clinical relevance for the identification of novel intervention targets.Accumulating evidence indicates that the tumor microenvironment plays a central regulatory role in prostate cancer initiation and progression. Among its components, inflammation, autophagy, and pyroptosis represent highly interconnected biological pathways that are deeply involved in tumor initiation, progression, immune modulation, and the development of therapeutic resistance. However, existing studies have largely focused on individual pathways, lacking a comprehensive understanding of their dynamic interplay and integrated regulatory networks.Chronic inflammation promotes tumor progression through sustained release of pro-inflammatory cytokines and immune cell infiltration, leading to genomic instability and aberrant activation of key signaling pathways. Autophagy exhibits a pronounced context-dependent role in prostate cancer, suppressing tumor initiation while paradoxically enhancing cancer cell survival and resistance under metabolic stress and therapeutic pressure. Pyroptosis, an inflammasome-dependent form of programmed cell death, can either facilitate immune evasion via inflammatory mediator release or activate antitumor immune responses, depending on the cellular and microenvironmental context.Notably, key signaling pathways such as NF-κB, mTOR, and AMPK serve as critical nodes linking inflammation, autophagy, and pyroptosis, collectively shaping the biological heterogeneity of prostate cancer and its response to therapy. A deeper understanding of the interactions and dynamic balance among inflammation, autophagy, and pyroptosis will not only address current gaps in the systemic mechanistic framework of prostate cancer research, but also advance our knowledge of its molecular pathology. Importantly, such insights may provide a solid theoretical foundation for the development of precision therapeutic strategies that concurrently target these pathways, thereby offering new avenues to overcome treatment resistance.