Our study establishes a clinically actionable amino acid metabolic signature and nomogram for PCa risk stratification, while suggesting FUS as a candidate therapeutic target. These findings bridge computational discovery with mechanistic validation, providing novel insights into the amino acid metabolic dependencies that govern prostate cancer (PCa) progression.
Finally, we discuss the predicted therapeutic approaches based on precision oncology to target and alter senescence using senolytics to eradicate aberrant senescent cells and senomorphics to target and adjust SASP. Addressing and regulating the plasticity of senescence is a significant and critical opportunity for improving the prognosis of prostate cancer, as well as guiding next-generation senescence-informed therapeutic approaches.