ABCG2 gene amplification and expression in esophageal cancer cells with acquired adriamycin resistance
ABCG2 gene amplification and expression in esophageal cancer cells with acquired adriamycin resistance
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DOI：
10.3892/mmr.2014.1949
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发表时间：
2014-04-01
影响因子：
3.4
通讯作者：
Guo, Jian Wen
中科院分区：
文献类型：
--
作者：
Liu, Liang;Zuo, Lian Fu;Guo, Jian Wen
化疗药物耐药性是癌症患者治疗失败的主要原因。多药耐药(MDR)的主要机制是药物外排转运体的过度表达，包括ATP结合盒转运体G2(ABCG2)。就我们所知，食道癌的多药耐药机制尚未被描述。从食道癌Eca109细胞株中，用L从0.002 ng/亩到0.02 ng/亩的浓度进行逐步筛选，获得了一株对阿霉素耐药的细胞系Eca109/ADM，其耐药性是Eca109细胞的3.29倍。与Eca109细胞相比，Eca109/ADM细胞中ABCG2基因的表达增强。逆转录-聚合酶链式反应(RT-PCR)、流式细胞仪和Western blotting检测Eca109/ADM细胞的特性。用逆转录聚合酶链式反应和流式细胞仪检测ABCG2的表达水平，用流式细胞仪检测药物外排效果。本研究检测了ABCG2与食管癌多药耐药的相关性。与Eca109细胞相比，Eca109/ADM细胞的ABCG2基因表达增强，药物外排作用增强。综上所述，本研究结果提示ABCG2在Eca109/ADM细胞中过表达导致药物外排，这可能是食道癌多药耐药的发生机制之一。
Resistance to chemotherapeutic agents is the main reason for treatment failure in patients with cancer. The primary mechanism of multidrug resistance (MDR) is the overexpression of drug efflux transporters, including ATP-binding cassette transporter G2 (ABCG2). To the best of our knowledge, the MDR mechanisms of esophageal cancer have not been described. An adriamycin (ADM)-resistant subline, Eca109/ADM, was generated from the Eca109 esophageal cancer cell line by a stepwise selection in ADM from 0.002 to 0.02 ng/mu l. The resulting subline, designated Eca109/ADM, revealed a 3.29-fold resistance against ADM compared with the Eca109 cell line. The ABCG2 gene expression in the Eca109/ADM cells was increased compared with that of the Eca109 cells. The cellular properties of the Eca109/ADM cells were detected by reverse transcription polymerase chain reaction (RT-PCR), flow cytometry and western blotting. The ABCG2 expression levels were detected by RT-PCR and flow cytometry, and the drug efflux effect was detected by flow cytometry. The present study detected the correlation between ABCG2 and the multidrug resistance of esophageal cancer. ABCG2 gene expression and the drug efflux effect of the Eca109/ADM cells were increased compared with those of the Eca109 cells. Collectively, the results of this study indicated that the overexpression of ABCG2 in the Eca109/ADM cells resulted in drug efflux, which may be responsible for the development of esophageal cancer MDR.