Naugler Willscott E, Karin Michael
Department of Medicine, Division of Gastroenterology and Hepatology, Oregon Health and Sciences University, Portland, USA.
Curr Opin Genet Dev. 2008 Feb;18(1):19-26. doi: 10.1016/j.gde.2008.01.020. Epub 2008 Apr 24.
A connection between inflammation and carcinogenesis has long been known, but the precise mechanisms are just beginning to be understood. NF-kappaB proteins, transcription factors which integrate stress signals and orchestrate immune responses, have also recently been linked to carcinogenesis. Hallmarks of cancer development include self-sufficiency in growth signals, insensitivity to growth-inhibitors, evasion of apoptosis, limitless replicative potential, tissue invasion and metastasis, and sustained angiogenesis. NF-kappaB signaling has been implicated in each of these hallmarks, and recent experimental studies have illuminated the mechanistic pathways by which NF-kappaB signaling contributes to these aspects of carcinogenesis. This review will focus on recent experimental data supporting the hypothesis that inflammation promotes carcinogenesis, and that NF-kappaB signaling is at the heart of such inflammation.
炎症与致癌作用之间的联系早已为人所知,但确切机制才刚刚开始被理解。核因子-κB(NF-κB)蛋白作为整合应激信号并协调免疫反应的转录因子,最近也被认为与致癌作用有关。癌症发展的标志包括生长信号的自给自足、对生长抑制剂不敏感、逃避细胞凋亡、无限增殖潜能、组织侵袭和转移以及持续的血管生成。NF-κB信号通路与上述每一个标志都有关联,最近的实验研究阐明了NF-κB信号通路促成致癌作用这些方面的机制途径。本综述将聚焦于支持炎症促进致癌作用以及NF-κB信号通路是这种炎症核心这一假说的最新实验数据。