Genomic analysis of drug resistant gastric cancer cell lines by combining mRNA and microRNA expression profiling

被引:28
作者
Chen, Zhangqian [1 ,2 ]
Zhang, Lin [1 ,2 ]
Xia, Limin [1 ,2 ]
Jin, Yangsheng [3 ]
Wu, Qing [3 ]
Guo, Hao [1 ,2 ]
Shang, Xin [1 ,2 ]
Dou, Jianhua [1 ,2 ]
Wu, Kaichun [1 ,2 ]
Nie, Yongzhan [1 ,2 ]
Fan, Daiming [1 ,2 ]
机构
[1] Fourth Mil Med Univ, State Key Lab Canc Biol, Xian 710032, Shaanxi, Peoples R China
[2] Fourth Mil Med Univ, Xijing Hosp Digest Dis, Xian 710032, Shaanxi, Peoples R China
[3] Shanghai Genechem Co Ltd, Bioinformat Dept, Shanghai 201203, Peoples R China
关键词
Gastric cancer; Multidrug resistance; Expression profiling; Mechanism; Therapeutic target; MULTIDRUG-RESISTANCE; LUNG-CANCER; MESENCHYMAL TRANSITION; ADENOCARCINOMA CELLS; TARGETING BCL2; GENES; CHEMOTHERAPY; CHEMORESISTANCE; MECHANISM; GROWTH;
D O I
10.1016/j.canlet.2014.04.010
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Understanding the mechanism underlying multidrug resistance and identifying effective targets that can overcome it is of critical importance. In this study, mRNA and miRNA expression profiling of the drug resistant sublines, SGC7901/VCR and SGC7901/ADR, and their parental gastric cancer cell line SGC7901 were performed. A significant number of genes and a limited subset of miRNAs were commonly dysregulated, which were further validated using qRT-PCR. GO and KEGG pathway analyses of the commonly dysregulated genes indicated that the MAPK signalling pathway may be involved in multidrug resistance, which was further validated using immunoblotting and MTT assay. Finally a primary multidrug resistance network in gastric cancer, consisting of the commonly dysregulated genes and miRNAs, was established and functional miRNA-mRNA pairs were identified. The commonly dysregulated genes and miRNAs identified in this study may represent good therapeutic targets and further study of these targets may increase our understanding of the mechanisms underlying multidrug resistance. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:43 / 51
页数:9
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