Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, KY 40506-0054, USA.
Curr Cancer Drug Targets. 2012 Nov 1;12(9):1160-72. doi: 10.2174/156800912803987931.
In this review, the role of nuclear factor-κB (NF-κB) in hepatocarcinogenesis is examined. The administration of several hepatic tumor promoters leads to the activation of NF-κB in the liver of rats and mice. Many studies support the hypothesis that the activation of NF-κB in the liver is inhibited by antioxidants. The role of NF-κB in hepatocarcinogenesis has been examined using NF-κB overexpression and knockout models. The role of NF-κB in liver carcinogenesis is complex; some models show that NF-κB contributes to carcinogenesis whereas others see no effect or an inhibition. Overall, although hepatic tumor promoting agents can activate NF-κB and this activation can be inhibited by antioxidants, the significance of this activation is unclear.
在这篇综述中,我们研究了核因子-κB(NF-κB)在肝癌发生中的作用。几种肝肿瘤促进剂的给药导致大鼠和小鼠肝脏中 NF-κB 的激活。许多研究支持这样的假设,即抗氧化剂可以抑制 NF-κB 在肝脏中的激活。已经使用 NF-κB 过表达和敲除模型来研究 NF-κB 在肝癌发生中的作用。NF-κB 在肝癌发生中的作用很复杂;一些模型表明 NF-κB 有助于致癌作用,而另一些模型则没有影响或抑制作用。总的来说,尽管肝肿瘤促进剂可以激活 NF-κB,并且这种激活可以被抗氧化剂抑制,但这种激活的意义尚不清楚。