Our results in vivo also indicated that greater Skp2–Foxa1–Pcna colocalization in prostate tumors of Pten/Trp53 mice, an in vivo model for advanced PCa, promoted PCa progression, whereas loss of Skp2 in Ptenpc−/−; Trp53pc−/−; Skp2−/− reduced tumor burden by stabilizing Foxa1 protein and luminal phenotypes while simultaneously decreasing Pcna levels. Here, SKP2 is linked to prostate neoplasm.