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首页> 外文期刊>Molecular and Cellular Biology >A Novel Transcription Complex That Selectively Modulates Apoptosis of Breast Cancer Cells through Regulation of FASTKD2
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A Novel Transcription Complex That Selectively Modulates Apoptosis of Breast Cancer Cells through Regulation of FASTKD2

机译：通过调节FASTKD2选择性调节乳腺癌细胞凋亡的新型转录复合体。

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We previously reported that expression of NRIF3 (nuclear receptor interacting factor-3) rapidly and selectively leads to apoptosis of breast cancer cells. DIF-1 (also known as interferon regulatory factor-2 binding protein 2 [IRF-2BP2]), the cellular target of NRIF3, was identified as a transcriptional repressor, and DIF-1 knockdown leads to apoptosis of breast cancer cells but not other cell types. Here, we identify IRF-2BP1 and EAP1 (enhanced at puberty 1) as important components of the DIF-1 complex mediating both complex stability and transcriptional repression. This interaction of DIF-1, IRF-2BP1, and EAP1 occurs through the conserved C4 zinc fingers of these proteins. Microarray studies were carried out in breast cancer cell lines engineered to conditionally and rapidly increase the levels of the death domain (DD1) region of NRIF3. The DIF-1 complex was found to repress FASTKD2, a putative proapoptotic gene, in breast cancer cells and to bind to the FASTKD2 gene by chromatin immunoprecipitation. FASTKD2 knockdown prevents apoptosis of breast cancer cells from NRIF3 expression or DIF-1 knockdown, while expression of FASTKD2 leads to apoptosis of both breast and nonbreast cancer cells. Thus, regulation of FASTKD2 by NRIF3 and the DIF-1 complex acts as a novel death switch that selectively modulates apoptosis in breast cancer.
机译：先前我们报道了NRIF3（核受体相互作用因子3）的表达迅速而选择性地导致乳腺癌细胞凋亡。 DIF-1（也称为干扰素调节因子2结合蛋白2 [IRF-2BP2]）是NRIF3的细胞靶标，被确定为转录阻遏物，而DIF-1敲低导致乳腺癌细胞凋亡，而其他方面则没有单元格类型。在这里，我们确定IRF-2BP1和EAP1（在青春期1时增强）是DIF-1复合物的重要组成部分，介导复合物稳定性和转录抑制。 DIF-1，IRF-2BP1和EAP1的这种相互作用通过这些蛋白质的保守C4锌指发生。微阵列研究是在乳腺癌细胞系中进行的，该细胞系被设计为有条件并迅速增加NRIF3死亡域（DD1）区域的水平。发现DIF-1复合物在乳腺癌细胞中阻遏推定的促凋亡基因FASTKD2，并通过染色质免疫沉淀与FASTKD2基因结合。 FASTKD2敲低可防止乳腺癌细胞因NRIF3表达或DIF-1敲低而凋亡，而FASTKD2的表达可导致乳腺癌和非乳腺癌细胞凋亡。因此，NRIF3和DIF-1复合物对FASTKD2的调节可作为一种新型的死亡开关，可以选择性地调节乳腺癌细胞的凋亡。

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