Transcriptomic analysis of human castration-resistant prostate cancer: Insights into novel therapeutic strategies.

Prostate cancer is a major cause of cancer-related deaths in men worldwide. Androgen deprivation therapy (ADT) is the standard treatment for advanced prostate cancer; however, disease progression to castration-resistant prostate cancer (CRPC) presents a significant therapeutic challenge. In this study, we employed transcriptomic analysis to investigate key genetic drivers of CRPC and identify novel therapeutic targets. Using RNA-seq data and bioinformatics tools, we identified differentially expressed genes (DEGs) associated with tumor progression, cytoskeletal dynamics, and immune modulation, including COL3A1, MYH4, FN1, ACTN1, and CALR. Functional enrichment analysis revealed significant involvement of actin-myosin filament sliding, calcium signaling, androgen receptor signaling, immune evasion, and metabolic pathways, underscoring their roles in CRPC progression and treatment resistance. Additionally, molecular docking studies demonstrated strong binding interactions between key CRPC-related genes (ABCC4 and FOLH1) and potential therapeutic ligands, including flutamide and N-acetyl glucosamine (NAG), highlighting their therapeutic potential in overcoming drug resistance. These findings provide novel insights into the molecular landscape of CRPC and support the development of precision-targeted therapies to improve patient outcomes.