EZH2 blockade by RNA interference inhibits growth of ovarian cancer by facilitating re-expression of p21waf1/cip1 and by inhibiting mutant p53

• Enhancer of zeste homolog 2 (EZH2) is abnormally elevated in ovarian cancer.
• EZH2 knockdown inhibited cell proliferation, colony formation, and cell invasion.
• EZH2 knockdown increased the apoptotic pathway and p21waf1/cip1 expression.
• Silencing of EZH2 inhibited mutant p53 protein and tumor xenograft growth.

The enhancer of zeste homolog 2 (EZH2) methyltransferase is a transcriptional repressor. EZH2 is abnormally elevated in epithelial ovarian cancer (EOC). We demonstrated that EZH2 knockdown inhibited cell growth, activated apoptosis, and enhanced chemosensitivity. Further, silencing of EZH2 resulted in re-expression of p21waf1/cip1 and down-regulation of mutant p53. Finally, EZH2 knockdown contributed to attenuated EOC growth in SCID mice.