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Regulation of Aurora B Expression by the Bromodomain Protein Brd4

机译：溴结构域蛋白Brd4调节极光B表达。

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The bromodomain protein Brd4 plays critical roles in cellular proliferation and cell cycle progression. In this study, we investigated the involvement of Brd4 in cell cycle regulation and observed aberrant chromosome segregation and failures in cytokinesis in cancer cells as well as in primary keratinocytes in which Brd4 has been knocked down by RNA interference. Suppression of Brd4 protein levels in proliferating cells decreased Aurora B protein and transcript levels and abolished its chromosomal distribution. In contrast, exogenous Brd4 expression stimulated Aurora B promoter reporter activity and upregulated endogenous Aurora B expression. Aurora B kinase is a chromosomal passenger protein that is essential for chromosome segregation and cytokinesis. Either overexpression of Aurora B or its inactivation can induce defects in centrosome function, spindle assembly, chromosome alignment, and cytokinesis in various cancer cells. The impaired regulation of Aurora B expression in human cells by Brd4 knockdown or overexpression coincided with mitotic catastrophe and multinucleation that are typically observed when Aurora B is inactivated or overexpressed. Overall, our data suggest that Brd4 is essential for the maintenance of the cell cycle progression mediated at least in part through the control of transcription of the Aurora B kinase cell cycle regulatory gene.
机译：溴结构域蛋白Brd4在细胞增殖和细胞周期进程中起关键作用。在这项研究中，我们调查了Brd4在细胞周期调控中的参与，并观察到异常的染色体分离和癌细胞以及原代角质形成细胞中胞质分裂的失败，在这些细胞中，Brd4被RNA干扰击倒。增殖细胞中Brd4蛋白水平的抑制降低了Aurora B蛋白和转录水平，并消除了其染色体分布。相比之下，外源性Brd4表达刺激Aurora B启动子报道分子活性并上调内源性Aurora B表达。 Aurora B激酶是一种染色体客体蛋白，对于染色体分离和胞质分裂是必不可少的。 Aurora B的过表达或其失活都可以在各种癌细胞中诱导中心体功能，纺锤体组装，染色体排列和胞质分裂的缺陷。 Brd4敲低或过表达会破坏人细胞中Aurora B的表达，这与有丝分裂灾难和多核现象相吻合，而Aurora B失活或过表达时通常会观察到。总体而言，我们的数据表明，Brd4对于维持至少部分通过控制Aurora B激酶细胞周期调节基因的转录介导的细胞周期进程至关重要。

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