AEG1 induces COX-2 expression via activation of NF-κB and AP-1 in hepatoma HepG2 cells  

AEG1通过激活NF-κB和AP-1诱导肝癌HepG2细胞COX-2表达(英文)

作　　者：Huan Deng Zhenzhen Zhou Wei Tu Yujia Xia Huanjun Huang De'an Tian 

机构地区：[1]Department of Gastroenterology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology

出　　处：《The Chinese-German Journal of Clinical Oncology》2013年第6期253-256,共4页中德临床肿瘤学杂志（英文版）

基　　金：Supported by grants from the National Science Foundation of China (No.81070333);the Natural Science Foundation of Hubei Province of China (No.2012FFB02318)

摘　　要：Objective： The aim of this study was to investigate whether astrecyte elevated gene 1 （AEG1） regulates COX-2 expression in human hepatoma HepG2 cells and related pathways involved in this process. Methods： Human hepatoma HepG2 cells were transfected with pcDNA3.1（-）-AEG1 plasmid or psilencer2.0-AEGl-shRNA1 plasmid to up/down-regulate AEG1 expression, pcDNA3.1（-） and psilencer 2.0 empty vector plasmids were transfected respectively as control. Real-time RT-PCR was carried out to measure the expression levels of AEG1 and COX-2 mRNA. The expression levels of AEG1 and COX-2 protein were detected by Western blot. NF-KB signaling was blocked by PDTC, and AP-1 signaling was blocked by curcumin. Results： AEG1 mRNA and protein levels were increased after pcDNA3.1（-）-AEG1 transfection, and decreased after psilencer2.0-AEGl-shRNAs transfection. COX-2 mRNA and protein levels were increased in AEGl-overexpressing cells and decreased in AEGl-knockdown cells. Phosphorylations of p65 and c-jun were up-regulated in AEGl-overexpressing cells. Both PDTC and curoumin reduced COX-2 expression in HepG2 cells with AEG1 overexpression. Conclusion： AEG1- overexpressing and -knockdown HepG2 cells are established successfully. AEG1 could induce COX-2 expression though activating NF-KB and AP-1 in human hepatoma HepG2 cells.

关 键 词：hepatocellular carcinoma astrocyte elevated gene 1（AEG1） COX-2 NF-ΚB AP-1 

分 类 号：R735.7[医药卫生—肿瘤]