Isolation and characterization of erlotinib-resistant human non-small cell lung cancer A549 cells

被引:8
作者
Ikeda, Ryuji [2 ]
Vermeulen, Lee C. [1 ,3 ]
Lau, Elim [4 ]
Jiang, Zhisheng [4 ]
Kavanaugh, Shannon M. [4 ]
Yamada, Katsushi [2 ]
Kolesar, Jill M. [1 ,4 ]
机构
[1] Univ Wisconsin, Sch Pharm, Div Pharma Practice, Madison, WI 53705 USA
[2] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Clin Pharm & Pharmacol, Kagoshima, Japan
[3] Univ Wisconsin, Hosp & Clin, Ctr Drug Policy, Madison, WI 53705 USA
[4] Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, Madison, WI 53705 USA
关键词
erlotinib; epidermal growth factor receptor; fibroblast growth factor 2; p21; GROWTH-FACTOR-RECEPTOR; PHASE-III TRIAL; ACQUIRED-RESISTANCE; THERAPY; EGFR; CHEMOTHERAPY; ANTAGONISTS; INHIBITORS; MUTATIONS; GEFITINIB;
D O I
10.3892/ol.2010.198
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Erlotinib, an epidermal growth factor receptor (EGER) tyrosine kinase inhibitor, is an effective therapy for non-small cell lung cancer (NSCLC). However, resistance to erlotinib reduces its efficacy. To investigate the basis of erlotinib resistance, we isolated erlotinib-resistant human NSCLC A549 cells, termed A549/ER cells. The A549/ER cells were found to be resistant to erlotinib, as well as paclitaxel and gemcitabine. We then performed a PCR array to investigate the resistance to erlotinib in A549/ER cells. EGFR expression in A549/ER cells was decreased compared to A549 cells. The expression of fibroblast growth factor 2 (FGF2) and p21 in A549/ER was increased when compared to A549 cells. Our results suggest that the down-regulation of EGFR and up-regulation of FGF2 is related to resistance to erlotinib in A549/ER cells.
引用
收藏
页码:91 / 94
页数:4
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