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NF-κB as node for signal amplification during weaning

机译：NF-κB作为断奶期间信号放大的节点

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摘要

Post-lactational involution has been reported to share common features with breast tumor development. A deep characterization of the signaling triggered after weaning would help to unveil the complex relationship between involution and breast cancer. NF-κB, a crucial factor in the involuting gland, might be an important regulatory node for signal amplification after weaning; however there is limited information about the identity of NF-κB-target genes and the molecular mechanisms leading to the selection of genes involved in a particular biological process. We identified 4532 target genes in mammary gland at 48h weaning, by genome-wide analysis of regions bound by RelA(p65)-NF- κB in vivo. It was found that among total RelA(p65)-NF-κB-enriched genes, only 268 bound the trans-activating complex p65/p300. Our results suggest that the latter represents a major complex preferentially involved in the modulation of the inflammatory response at 48h of mammary gland involution. A genome-wide factor location analysis revealed that p65-binding had a heterogeneous distribution while the complex of p65 and its co-activator p300 were mainly bound to proximal promoters near transcription start sites. Moreover, our computational analysis predicts the existence of cooperating elements on RelA-NF-κB/p300-enriched genes that could explain preferential binding and modulation of gene expression during mammary gland involution.
机译：据报道，胎后消退与乳腺肿瘤的发展具有共同的特征。断奶后触发信号的深入表征将有助于揭示内卷化与乳腺癌之间的复杂关系。 NF-κB是渐开线腺体中的关键因素，可能是断奶后信号放大的重要调控节点。然而，关于NF-κB-靶基因的身份以及导致选择涉及特定生物学过程的基因的分子机制的信息有限。通过在体内通过RelA（p65）-NF-κB结合的区域进行全基因组分析，我们在断奶48h时在乳腺中鉴定了4532个靶基因。发现在全部富含RelA（p65）-NF-κB的基因中，只有268结合了反式激活复合物p65 / p300。我们的研究结果表明，后者代表了一种主要复合物，优先参与乳腺退化48h时炎症反应的调节。全基因组因子定位分析表明，p65结合具有异质分布，而p65及其共激活因子p300的复合体主要结合到转录起始位点附近的近端启动子。此外，我们的计算分析预测，在富含RelA-NF-κB/ p300的基因上存在协作元件，这可能解释了乳腺退化过程中基因表达的优先结合和调控。

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