| Literature DB >> 27717711 |
Qiong Duan1, Yi Xiao1, Lingyan Zhu2, Zhenzhen Liu1, Xiaoxiao Mao3, Zhengxiang Zhou1, Chaonan Liao4, Jinxing Cai4, Fulian Huang5, Zehao Liu6, Jian Zeng7, Ke Xia1, Cheng Chang8, Jun Qi9, Zihua Chen10, He Huang11, Tianlun Yang12.
Abstract
Transcriptional coactivator with PDZ-binding motif (TAZ) is a key transcriptional mediator of Hippo signaling that has been recently reported to mediate Wnt-activated transcription and serve as a component to suppress canonical Wnt/β-catenin activity. The Bromodomain and Extra-terminal domain (BET) family of proteins can recognize the acetylated lysine chain on histones and plays a critical role in transcriptional regulation. However, the mechanisms underlying transcriptional repression by the BET bromodomain are poorly understood. Here, we found that BET bromodomain inhibition upregulated TAZ protein and its transcriptional output, independent of its well-established role as a mediator of Hippo and Wnt signaling. Additionally, JQ1, a synthetic BET inhibitor, suppressed Wnt/β-catenin activity by upregulating TAZ. Although JQ1 upregulated TAZ, which is known to promote cell proliferation, it drastically suppressed the growth of colon cancer cells by inducing cell cycle arrest. Collectively, our study identified an unexpected transcriptional repression function of the BET bromodomain and a novel mechanism for TAZ upregulation.Entities:
Keywords: Bromodomain and extra-terminal domain protein (BET); Colon cancer; TAZ; β-Catenin
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Year: 2016 PMID： 27717711 DOI： 10.1016/j.bbagrm.2016.10.001
Source DB: PubMed Journal: Biochim Biophys Acta ISSN： 0006-3002