Role of ABCG2 in erlotinib resistance in non-small-cell lung cancer

张靖; 马虎; 韩静; 李雪涛; 陈正堂

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Role of ABCG2 in erlotinib resistance in non-small-cell lung cancer

更新时间：2026-01-09

- Role of ABCG2 in erlotinib resistance in non-small-cell lung cancer
- Journal of Army Medical University Vol. 36, Issue 10, Pages: 987-991(2014)
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  CLC： R434.2;R966;R979.19
- Published：2014
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张靖,马虎,韩静,李雪涛,陈正堂.ABCG2在非小细胞肺癌厄洛替尼耐药中的作用[J].陆军军医大学学报(原第三军医大学学报),2014,36(10):987-991.

　Zhang Jing,Ma Hu,Han Jing,Li Xuetao,Cheng Zhengtang.Role of ABCG2 in erlotinib resistance in non-small-cell lung cancer[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(10):987-991.
张靖,马虎,韩静,李雪涛,陈正堂.ABCG2在非小细胞肺癌厄洛替尼耐药中的作用[J].陆军军医大学学报(原第三军医大学学报),2014,36(10):987-991. DOI：

　Zhang Jing,Ma Hu,Han Jing,Li Xuetao,Cheng Zhengtang.Role of ABCG2 in erlotinib resistance in non-small-cell lung cancer[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(10):987-991. DOI：

摘要

目的探讨ABCG2在非小细胞肺癌厄洛替尼耐药中的作用。方法厄洛替尼不同浓度（1、5、25 μmol/L)处理A549细胞及其获得性耐厄洛替尼细胞(A549/ER)12、24、48 h后

荧光实时定量PCR观察ABCG2 mRNA表达变化，Western blot检测p-AKT、ABCG2蛋白表达变化。PI3K/AKT通路激活剂（IGF-1）和抑制剂（LY294002）分别作用于A549细胞及A549/ER细胞24 h后，荧光实时定量PCR和Western blot方法分别检测ABCG2 mRNA及p-AKT、ABCG2蛋白表达变化。流式细胞仪检测加入IGF-1和LY294002后ABCG2外排作用。结果与未加入厄洛替尼的A549、A549/ER细胞相比，厄洛替尼（1、5、25 μmol/L)作用12、24、48 h后，随着剂量的增加和作用时间的延长，ABCG2的表达与p-AKT水平呈正相关。加入IGF-1 24 h后，A549细胞中ABCG2表达量升高，而加入LY294002的A549/ER细胞，ABCG2表达量下降，并且IGF-1作用24 h后ABCG2外排明显增高。LY294002作用24 h后A549/ER细胞ABCG2外排明显降低。结论 ABCG2经由PI3K/AKT信号通路介导非小细胞肺癌中厄洛潜尼耐药，且阻断PI3K/AKT通路可逆转由ABCG2介导的耐药。

Abstract

Objective To determine the role of ATP-binding cassette sub-family G member 2 (ABCG2) in erlotinib resistance in non-small-cell lung cancer. Methods A549 cells and acquired erlotinib-resistant A549 cells (A549/ER) were separately treated with different concentrations of erlotinib for 12

24 and 48 h respectively. Real-time PCR and Western blotting were used to observe the changes of ABCG2 expressions at mRNA and protein levels. The activator (IGF-1) and inhibitor (LY294002) of PI3K/AKT pathway were used to treat A549 cells and A549/ER cells for 24 h

respectively. The expression changes of ABCG2 mRNA and p-AKT and ABCG2 were observed by real-time PCR and Western blot analysis. The efflux effect of ABCG2 after IGF-1 and LY294002 treatment was detected by flow cytometry. Results Compared with the A549 and A549/ER cells without erlotinib treatment

after treated by erlotinib (1

5 and 25 μmol/L) for 12

24 and 48 h

the expression of ABCG2 and inhibition or activation of PI3K/AKT signaling pathway were positively correlated with the increase of dosage and treatment time. The expression level of ABCG2 was increased in A549 cells treated with IGF-1 for 24 h and decreased in A549/ER cells treated with LY294002. In addition

the efflux effect of ABCG2 was significantly increased after IGF-1 treatment for 24 h and significantly decreased after LY294002 treatment for 24 h. Conclusion ABCG2 mediates erlotinib resistance in non-small-cell lung cancer by PI3K/AKT pathway

and blocking the pathway will reverse the drug resistance.

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