In prostate cancer, we molecularly characterized the H19/cell adhesion molecules’ circuitry, in which H19 acts as a transcriptional repressor of specific cell adhesion molecules, including E-cadherin and β4 integrin, by recruiting the EZH2 polycomb subunit on the promoter region and increasing the H3K27me3 level. This evidence concerns the gene H19 and prostate carcinoma.