泛素编辑酶A20改变炎症状态及调控NF-κB信号通路逆转癌症的研究进展  

The progress of A20 alter the inflammatory state and regulate the NF-κB signaling pathway to reverse the progression of cancer

作　　者：周昕 安东建[2] 胡锦跃[3] Zhou Xin;An Dongjian;Hu Jinyue(University of South China, Hunan Hengyang 421001, China;Changsha Central Hospital, Hunan Changsha 410004, China;Central Laboratory of Changsha Central Hospital, Hunan Changsha 410004, China.)

机构地区：[1]南华大学,湖南衡阳421001 [2]长沙市中心医院,湖南长沙410004 [3]长沙市中心医院中心实验室,湖南长沙410004

出　　处：《现代肿瘤医学》2018年第9期1447-1450,共4页Journal of Modern Oncology

基　　金：国家自然科学基金(编号:81172042)

摘　　要：近来的研究数据极大地支持了慢性炎症是癌症发展的关键组成部分的概念。许多癌症来自感染部位,促炎细胞因子协调肿瘤微环境并参与肿瘤过程,通过促进肿瘤细胞增殖、存活、侵袭和转移。A20(也称为RNFAIP3)是泛素编辑酶,作为有效的抗炎信号分子,可以限制多个细胞内信号级联。最近的报道已将A20鉴定为各种癌症中关键的肿瘤抑制因子。本文就A20在炎症信号级联调控中的作用作一综述,并解释了A20如何通过抑制炎症反应来调节癌症进展。Recent data have expanded the concept that chronic inflammation is a critical component of cancer development. Many cancers arise from the sites of infection,and pro-inflammatory cytokines orchestrate tumor microenvironment to participant in the neoplastic process,fostering proliferation,survival,invasion and metastasis. A20（ also known as RNFAIP3） is an ubiquitin-editing enzyme,and functions as a potent anti-inflammatory signaling molecule to restrict multiple intracellular signaling cascades. Recent reports have identified A20 as a crucial tumor suppressor in various cancers. In this review we summarize the roles of A20 in the modulation of inflammatory signaling cascades,and explain how A20 regulates cancer progress by inhibition of inflammatory response.

关 键 词：A20 NF-ΚB 肿瘤 信号传导 

分 类 号：R730[医药卫生—肿瘤]