Mechanistically, EZH2 overexpression promotes prostate cancer development by silencing ADRB2, a ß-adrenergic receptor; loss of ADRB2 expression induces cell invasion in benign prostate cells, whereas its constitutive expression counteracts the metastatic and proliferative effects induced by EZH2 overexpression. Here, ADRB2 is linked to prostate cancer.