Wedelolactone disrupts the interaction of EZH2-EED complex and inhibits PRC2-dependent cancer

نویسندگان

  • Huiming Chen
  • Shijuan Gao
  • Jiandong Li
  • Dong Liu
  • Chunjie Sheng
  • Chen Yao
  • Wei Jiang
  • Jiaoxiang Wu
  • Shuai Chen
  • Wenlin Huang
چکیده

Polycomb repressive complex 2 (PRC2), which is responsible for the trimethylation of H3K27 (H3K27me3), plays a part in tumorigenesis, development and/or maintenance of adult tissue specificity. The pivotal role of PRC2 in cancer makes it a therapeutic target for epigenetic cancer therapy. However, natural compounds targeting the enhancer of zeste homolog 2 (EZH2) - embryonic ectoderm development (EED) interaction to disable PRC2 complex are scarcely reported. Here, we reported the screening and identification of natural compounds which could disrupt the EZH2-EED interaction. One of these compounds, wedelolactone, binds to EED with a high affinity (KD = 2.82 μM), blocks the EZH2-EED interaction in vitro, induces the degradation of PRC2 core components and modulates the expression of detected PRC2 downstream targets and cancer-related genes. Furthermore, some PRC2-dependent cancer cells undergone growth arrest upon treatment with wedelolactone. Thus, wedelolactone and its derivatives which target the EZH2-EED interaction could be candidates for the treatment of PRC2-dependent cancer.

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عنوان ژورنال:

دوره 6  شماره 

صفحات  -

تاریخ انتشار 2015