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核因子-κB与癌症识别靶点及机制

NF-kappaB and cancer-identifying targets and mechanisms.

作者信息

Naugler Willscott E, Karin Michael

机构信息

Department of Medicine, Division of Gastroenterology and Hepatology, Oregon Health and Sciences University, Portland, USA.

出版信息

Curr Opin Genet Dev. 2008 Feb;18(1):19-26. doi: 10.1016/j.gde.2008.01.020. Epub 2008 Apr 24.

Abstract

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.

摘要

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。

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