Camptothecin and cisplatin upregulate ABCG2 and MRP2 expression by activating the ATMUNF-κB pathway in lung cancer cells

被引:48
作者
Ke, Shi Zhong [1 ]
Ni, Xiao Yan [1 ]
Zhang, Yue Hua [1 ]
Wang, Yi Nan [1 ]
Wu, Bin [2 ]
Gao, Feng Guang [1 ]
机构
[1] Xiamen Univ, Coll Med, Dept Immunol, Xiamen 361005, Peoples R China
[2] Shanghai Jiao Tong Univ, Affiliated Renji Hosp, Dept Pharmacol, Shanghai 200030, Peoples R China
基金
中国国家自然科学基金;
关键词
ataxia telangietisa mutanted; NF-kappa B; ABCG2; MRP2; lung cancer; INTERSTRAND CROSS-LINKS; MULTIDRUG-RESISTANCE; DNA-DAMAGE; IN-VITRO; ATAXIA-TELANGIECTASIA; DRUG-RESISTANCE; DENDRITIC CELLS; PROTEIN-KINASE; THERAPY; OVEREXPRESSION;
D O I
10.3892/ijo.2013.1805
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Multidrug resistance (MDR) formation is an important problem in lung cancer chemotherapy. Our study showed that both camptothecin and cisplatin could not only induce ATM and NF-kappa B activation but also upregulate expression of the MDR-related genes ABCG2, MRP2 in NCI-H446 cells. Moreover, camptothecin and cisplatin-induced ABCG2 and MRP2 upregulation could be impaired by ATM and NF-kappa B inhibitors, indicating a relationship between ATM, NF-kappa B activation and MDR formation in lung cancer chemotherapy. Our study indicates that ATM may serve as a potential molecular target for MDR formation in lung cancer chemotherapy.
引用
收藏
页码:1289 / 1296
页数:8
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