| Literature DB >> 23236167 |
Wei Qi1, HoMan Chan, Lin Teng, Ling Li, Shannon Chuai, Ruipeng Zhang, Jue Zeng, Min Li, Hong Fan, Ying Lin, Justin Gu, Ophelia Ardayfio, Ji-Hu Zhang, Xiaoxia Yan, Jialuo Fang, Yuan Mi, Man Zhang, Tao Zhou, Grace Feng, Zijun Chen, Guobin Li, Teddy Yang, Kehao Zhao, Xianghui Liu, Zhengtian Yu, Chris X Lu, Peter Atadja, En Li.
Abstract
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.Entities:
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Year: 2012 PMID: 23236167 PMCID: PMC3535655 DOI: 10.1073/pnas.1210371110
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205