China Novartis Institutes for BioMedical Research, Shanghai 201203, China.
Proc Natl Acad Sci U S A. 2012 Dec 26;109(52):21360-5. doi: 10.1073/pnas.1210371110. Epub 2012 Dec 10.
Ezh2 (Enhancer of zeste homolog 2) protein is the enzymatic component of the Polycomb repressive complex 2 (PRC2), which represses gene expression by methylating lysine 27 of histone H3 (H3K27) and regulates cell proliferation and differentiation during embryonic development. Recently, hot-spot mutations of Ezh2 were identified in diffused large B-cell lymphomas and follicular lymphomas. To investigate if tumor growth is dependent on the enzymatic activity of Ezh2, we developed a potent and selective small molecule inhibitor, EI1, which inhibits the enzymatic activity of Ezh2 through direct binding to the enzyme and competing with the methyl group donor S-Adenosyl methionine. EI1-treated cells exhibit genome-wide loss of H3K27 methylation and activation of PRC2 target genes. Furthermore, inhibition of Ezh2 by EI1 in diffused large B-cell lymphomas cells carrying the Y641 mutations results in decreased proliferation, cell cycle arrest, and apoptosis. These results provide strong validation of Ezh2 as a potential therapeutic target for the treatment of cancer.
Ezh2(增强子结合锌指蛋白 2)蛋白是多梳抑制复合物 2(PRC2)的酶成分,通过甲基化组蛋白 H3 的赖氨酸 27(H3K27)来抑制基因表达,并在胚胎发育过程中调节细胞增殖和分化。最近,在弥漫性大 B 细胞淋巴瘤和滤泡性淋巴瘤中鉴定出 Ezh2 的热点突变。为了研究肿瘤生长是否依赖于 Ezh2 的酶活性,我们开发了一种有效的、选择性的小分子抑制剂 EI1,它通过直接与酶结合并与甲基供体 S-腺苷甲硫氨酸竞争来抑制 Ezh2 的酶活性。EI1 处理的细胞表现出全基因组范围内的 H3K27 甲基化丧失和 PRC2 靶基因的激活。此外,在携带 Y641 突变的弥漫性大 B 细胞淋巴瘤细胞中,EI1 抑制 Ezh2 导致增殖减少、细胞周期停滞和凋亡。这些结果为 Ezh2 作为癌症治疗的潜在治疗靶点提供了强有力的验证。