镍暴露通过细胞凋亡、自噬诱导肺癌发生及相关信号通路  

Nickel exposure induces lung cancer through apoptosis and autophagy and related signaling pathways

作　　者：徐虹 朱晓晓 张顺 蔡挺 XU Hong;ZHU Xiaoxiao;ZHANG Shun;CAI Ting(Ningbo University School of Medicine,Ningbo 315000,China;Medical Experimental Department of the Huamei Hospital,University of Chinese Academy of Sciences,Ningbo 315000,China)

机构地区：[1]宁波大学医学院,宁波315000 [2]中国科学院大学宁波华美医院医学实验部,宁波315000

出　　处：《生命的化学》2020年第10期1715-1721,共7页Chemistry of Life

基　　金：浙江省自然科学基金项目(LY15H160046);宁波市科技创新团队项目(2011B82016)。

摘　　要：镍(nickel)是一种众所周知的有毒金属,在生产、回收和处置过程中导致了广泛的环境污染。流行病学及动物实验已经证明,镍及其化合物暴露会增加肺癌风险。细胞凋亡和自噬是维持细胞内稳态的两种重要的分子机制,当两者出现异常调节时可能会诱发癌变。近年来,镍致肺癌机制的研究受到广泛关注,已证实细胞的凋亡及自噬过程参与其中,且两者可能存在相互调节关系。本文就镍暴露通过细胞凋亡、自噬诱导肺癌发生的研究进展进行综述,并着重讨论了丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)信号通路、核因子-κB(nuclear factor-κB,NF-κB)信号通路、磷脂酰肌醇3-激酶/蛋白激酶B(phosphoinositide 3-kinase/protein kinase B,PI3K/AKT)信号通路、p53信号通路对镍暴露致肺癌的意义。Nickel is a well-known toxic metal,which leads to extensive environmental pollution in the process of production,recovery and disposal.Epidemiological and animal experiments have shown that exposure to nickel and its compounds increases the risk of lung cancer.Apoptosis and autophagy are two important molecular mechanisms for maintaining intracellular homeostasis,which may induce carcinogenesis when they are abnormally regulated.In recent years,the research on the mechanism of nickel-induced lung cancer has attracted much attention.It has been confirmed that apoptosis and autophagy are involved in the process,and there may exist mutual interaction between apoptosis and autophagy.This work reviews the research progress on lung cancer induced by nickel exposure through apoptosis and autophagy,and focuses on discussion of the significance of mitogen-activated protein kinase(MAPK)signaling pathway,nuclear factor-κB(NF-κB)signaling pathway,phosphoinositide 3-kinase/protein kinase B(PI3K/AKT)signaling pathway and p53 signaling pathway to lung cancer induced by nickel exposure.

关 键 词：镍 肺癌 凋亡 自噬 信号通路 

分 类 号：R734.2[医药卫生—肿瘤] R114[医药卫生—临床医学]