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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 

作者机构:Department of GastroenterologyTongji HospitalTongji Medical CollegeHuazhong University of Science and Technology 

出 版 物:《The Chinese-German Journal of Clinical Oncology》 (中德临床肿瘤学杂志(英文版))

年 卷 期:2013年第12卷第6期

页      面:253-256页

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

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) 

主  题:hepatocellular carcinoma astrocyte elevated gene 1(AEG1) COX-2 NF-κB AP-1 

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.

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