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The complexity of NF-κB signaling in inflammation and cancer

机译：炎症和癌症中NF-κB信号传导的复杂性

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The NF-κB family of transcription factors has an essential role in inflammation and innate immunity. Furthermore, NF-κB is increasingly recognized as a crucial player in many steps of cancer initiation and progression. During these latter processes NF-κB cooperates with multiple other signaling molecules and pathways. Prominent nodes of crosstalk are mediated by other transcription factors such as STAT3 and p53 or the ETS related gene ERG. These transcription factors either directly interact with NF-κB subunits or affect NF-κB target genes. Crosstalk can also occur through different kinases, such as GSK3 -β, p38, or PI3K , which modulate NF-κB transcriptional activity or affect upstream signaling pathways. Other classes of molecules that act as nodes of crosstalk are reactive oxygen species and miRNAs. In this review, we provide an overview of the most relevant modes of crosstalk and cooperativity between NF-κB and other signaling molecules during inflammation and cancer.
机译：NF-κB转录因子家族在炎症和先天免疫中起着至关重要的作用。此外，NF-κB在癌症的起始和发展的许多步骤中被越来越多地认为是至关重要的参与者。在后面的过程中，NF-κB与多种其他信号分子和途径协同作用。串扰的突出节点由其他转录因子（例如STAT3和p53或ETS相关基因ERG）介导。这些转录因子要么直接与NF-κB亚基相互作用，要么影响NF-κB靶基因。串扰也可以通过不同的激酶（例如GSK3-β，p38或PI3K）发生，这些激酶调节NF-κB转录活性或影响上游信号通路。充当串扰节点的其他种类的分子是活性氧和miRNA。在这篇综述中，我们概述了炎症和癌症期间NF-κB和其他信号分子之间最相关的串扰和协同作用模式。

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