通过 RNA 干扰抑制 EZH2 可促进 p21(waf1/cip1) 的重新表达并抑制突变型 p53，从而抑制卵巢癌细胞的生长。

EZH2 blockade by RNA interference inhibits growth of ovarian cancer by facilitating re-expression of p21(waf1/cip1) and by inhibiting mutant p53.

机构信息

Laboratory of Surgical Oncology & Developmental Therapeutics, Department of Surgery, Wayne State University, Detroit, MI 48201, USA.

出版信息

Cancer Lett. 2013 Aug 9;336(1):53-60. doi: 10.1016/j.canlet.2013.04.012. Epub 2013 Apr 18.

DOI:10.1016/j.canlet.2013.04.012

PMID:23603558

Abstract

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 p21(waf1/cip1) and down-regulation of mutant p53. Finally, EZH2 knockdown contributed to attenuated EOC growth in SCID mice.

摘要

EZH2 是一种转录抑制因子，其同源物增强子的结合蛋白 2 (EZH2) 甲基转移酶。EZH2 在卵巢上皮性癌（EOC）中异常升高。我们证明，EZH2 敲低可抑制细胞生长、激活细胞凋亡并增强化疗敏感性。此外，EZH2 的沉默导致 p21(waf1/cip1) 的重新表达和突变型 p53 的下调。最后，EZH2 敲低有助于减弱 SCID 小鼠中的 EOC 生长。