While the expression of CDKN1A can be regulated via both TP53-dependent and TP53-independent/cell cycle-dependent mechanisms25, and the dynamic between CDKN1A expression and cell cycle progression in prostate cancer is complicated26, these results suggest that CDKN1A expression in the LNCaP cell model is predominantly via the p53-dependent mechanism, and that endogenous p53 likely provides an inherent barrier to LNCaP cells’ proliferation and advancement to castration-resistant growth. Here, TP53 is linked to prostate carcinoma.