CDH1 and renal cell carcinoma: Mechanistically, the activity of MALAT1 in transcriptional regulation showed that MALAT1-knockdown inhibited the oncogenic function in RCC and consistently depleted histone methyltransferase enhancer of zeste homology 2 (EZH2), a histone lysine N-methyltransferase enzyme (EC 2.1.1.43), resulting in the inhibition of the EMT through the recovery of E-cadherin and a downregulation of β-catenin [40].