Both models showed reduced tumor growth (WT: 492.64 ± 143.16 mm3; uPA–/–: 82.19 ± 59.01 mm3; UK122: 169.13 ± 104.96 mm3; Figures 2A-C) and prolonged survival (p<0.05; Figure 2D), with the genetic knockout exhibiting superior efficacy to pharmacological inhibition, collectively establishing that uPA deficiency inhibited prostate cancer progression. This evidence concerns the gene PLAU and neoplasm.