De Bosscher K, Vanden Berghe W, Haegeman G
Laboratory for Eukaryotic Gene Expression and Signal Transduction (LEGEST), Department of Molecular Biology, Ghent University, Gent, Belgium.
Oncogene. 2006 Oct 30;25(51):6868-86. doi: 10.1038/sj.onc.1209935.
A variety of studies have shown that some activated nuclear receptors (NRs), especially the glucorticoid receptor, the estrogen receptor and peroxisome proliferator-activated receptor, can inhibit the activity of the transcription factor nuclear factor kappaB (NF-kappaB), which plays a key role in the control of genes involved in inflammation, cell proliferation and apoptosis. This review describes the molecular mechanisms of cross-talk between NRs and NF-kappaB and the biological relevance of this cross-talk. The importance and mechanistic aspects of selective NR modulation are discussed. Also included are future research prospects, which will lead to a new era in the field of NR research with the aim of specifically inhibiting NF-kappaB-driven gene expression for anti-inflammatory, anti-tumor and immune-modulatory purposes.
大量研究表明，一些活化的核受体（NRs），特别是糖皮质激素受体、雌激素受体和过氧化物酶体增殖物激活受体，能够抑制转录因子核因子κB（NF-κB）的活性，NF-κB在控制参与炎症、细胞增殖和凋亡的基因方面起着关键作用。本综述描述了NRs与NF-κB之间相互作用的分子机制以及这种相互作用的生物学意义。讨论了选择性NR调节的重要性和机制方面。还包括未来的研究前景，这将引领NR研究领域进入一个新时代，旨在特异性抑制NF-κB驱动的基因表达以实现抗炎、抗肿瘤和免疫调节目的。
