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GATA3和ZEB2的核抑制程序的相互反馈环路的失调导致乳腺癌转移

Dysfunction of the Reciprocal Feedback Loop between GATA3- and ZEB2-Nucleated Repression Programs Contributes to Breast Cancer Metastasis

来源:Scopus 发布时间:2015-8-20
作者:Si W., Huang W., Zheng Y., Yang Y., Liu X., Shan L., Zhou X., Wang Y., Su D., Gao J., Yan R., Han X., Li W., He L., Shi L., Xuan C., Liang J., Sun L., Wang Y., Shang Y.
机构: 北京大学恶性肿瘤发病机制及转化研究教育部重点实验室,蛋白质翻译后修饰和细胞功能北京市重点实验室,北京大学健康科学中心 生物化学和分子生物学系
期刊: CANCER CELL2015年6月6期27卷

How loss-of-function of GATA3 contributes to the development of breast cancer is poorly understood. Here, we report that GATA3 nucleates a transcription repression program composed of G9A and MTA3-, but not MTA1- or MTA2-, constituted NuRD complex. Genome-wide analysis of the GATA3/G9A/NuRD(MTA3) targets identified a cohort of genes including ZEB2 that are critically involved in epithelial-to-mesenchymal transition and cell invasion. We demonstrate that the GATA3/G9A/NuRD(MTA3) complex inhibits the invasive potential of breast cancer cells invitro and suppresses breast cancer metastasis invivo. Strikingly, the expression of GATA3, G9A, and MTA3 is concurrently downregulated during breast cancer progression, leading to an elevated expression of ZEB2, which, in turn, represses the expression of G9A and MTA3 through the recruitment of G9A/NuRD(MTA1). © 2015 Elsevier Inc.

通讯作者: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, China
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