Department of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University Vienna, Schwarzspanierstraße 17, 1090 Vienna, Austria.
Mol Cancer. 2013 Aug 2;12:86. doi: 10.1186/1476-4598-12-86.
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.
NF-κB 转录因子家族在炎症和先天免疫中具有重要作用。此外，NF-κB 越来越被认为是癌症发生和发展的许多步骤中的关键参与者。在这些过程中，NF-κB 与其他多种信号分子和途径合作。其他转录因子（如 STAT3 和 p53 或 ETS 相关基因 ERG）介导的串扰主要节点。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发生，例如 GSK3-β、p38 或 PI3K，它们调节 NF-κB 的转录活性或影响上游信号通路。作为串扰节点的其他类分子是活性氧和 miRNAs。在这篇综述中，我们概述了 NF-κB 与其他信号分子在炎症和癌症中的串扰和协同作用的最相关模式。
Zotero 插件
