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首页> 外文期刊>Cancer Cell >Dysfunction of the Reciprocal Feedback Loop between GATA3-and ZEB2-Nucleated Repression Programs Contributes to Breast Cancer Metastasis
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Dysfunction of the Reciprocal Feedback Loop between GATA3-and ZEB2-Nucleated Repression Programs Contributes to Breast Cancer Metastasis

机译：GATA3和ZEB2核抑制程序之间的相互反馈回路的功能障碍导致乳腺癌转移。

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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 in vitro and suppresses breast cancer metastasis in vivo. 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).
机译：人们对GATA3的功能丧失如何促进乳腺癌的发展知之甚少。在这里，我们报告说，GATA3形成了由G9A和MTA3-（但不是MTA1-或MTA2-）组成的NuRD复合物组成的转录阻遏程序。对GATA3 / G9A / NuRD（MTA3）目标的全基因组分析确定了包括ZEB2在内的一系列基因，这些基因与上皮向间充质转化和细胞侵袭至关重要。我们证明，GATA3 / G9A / NuRD（MTA3）复合物在体外抑制乳腺癌细胞的侵袭潜力，并在体内抑制乳腺癌转移。令人惊讶的是，在乳腺癌进展过程中，GATA3，G9A和MTA3的表达同时下调，导致ZEB2表达升高，进而通过募集G9A / NuRD（MTA1）抑制G9A和MTA3的表达。

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