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首页> 外文期刊>Molecular and Cellular Biology >CBP Mediates NF-κB-Dependent Histone Acetylation and Estrogen Receptor Recruitment to an Estrogen Response Element in the BIRC3 Promoter
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CBP Mediates NF-κB-Dependent Histone Acetylation and Estrogen Receptor Recruitment to an Estrogen Response Element in the BIRC3 Promoter

机译：CBP介导NF-κB依赖性组蛋白乙酰化和BIRC3启动子中雌激素反应元件的雌激素受体募集。

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Estrogen receptor (ER) and NF-κB are transcription factors with profound effects on breast cancer cell proliferation and survival. While many studies demonstrate that ER and NF-κB can repress each other, we previously identified a gene signature that is synergistically upregulated by these two factors in more aggressive luminal B breast tumors. Herein, we examine a novel mechanism of cross talk between ER and NF-κB that results in the upregulation of the antiapoptotic gene BIRC3 (also known as cIAP2). We demonstrate that NF-κB, acting through two response elements, is required for ER recruitment to an adjacent estrogen response element (ERE) in the BIRC3 promoter. This effect is accompanied by a major increase in NF-κB-dependent histone acetylation around the ERE. Interestingly, CBP, a histone acetyltransferase previously implicated in repressive interactions between ER and NF-κB, plays a permissive role by promoting histone acetylation and ER recruitment, as well as enhanced expression of BIRC3. These findings suggest a new gene regulatory mechanism by which inflammation and NF-κB activation can influence ER recruitment to inherently inactive ER binding sites. This fine-tuning mechanism may explain how two factors that generally repress each other's activity may work together on certain genes to promote breast cancer cell survival and tumor progression.
机译：雌激素受体（ER）和NF-κB是对乳腺癌细胞增殖和存活产生深远影响的转录因子。尽管许多研究表明ER和NF-κB可以相互抑制，但我们先前发现了在更具侵袭性的管腔B型乳腺肿瘤中这两个因素协同上调的基因标记。在本文中，我们研究了ER与NF-κB之间的一种新的串扰机制，该机制导致抗凋亡基因 BIRC3 （也称为 cIAP2 ）上调。我们证明，通过 BIRC3 启动子将ER募集到相邻的雌激素响应元件（ERE）时，需要通过两个响应元件起作用的NF-κB。该作用伴随着ERE周围NF-κB依赖性组蛋白乙酰化的大量增加。有趣的是，CBP是一种先前与ER和NF-κB之间的阻抑相互作用有关的组蛋白乙酰转移酶，通过促进组蛋白乙酰化和ER募集以及增强 BIRC3 的表达而发挥了宽容的作用。这些发现暗示了一种新的基因调节机制，炎症和NF-κB激活可通过这种机制调节内质网向内在无活性的内质网结合位点的募集。这种微调机制可以解释通常抑制彼此活动的两个因素如何共同作用于某些基因，从而促进乳腺癌细胞的存活和肿瘤的进展。

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