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基因芯片筛选CD133+/CD133-肺腺癌细胞中新的耐药基因

王红艳 郑少秋 涂永生 张雅洁

中国肺癌杂志Issue(6):437-443,7.
中国肺癌杂志Issue(6):437-443,7.DOI:10.3779/j.issn.1009-3419.2014.06.01

基因芯片筛选CD133+/CD133-肺腺癌细胞中新的耐药基因

Screening and Identiifcation of Novel Drug-resistant Genes in CD133+and CD133-Lung Adenosarcoma Cells Using cDNA Microarray

王红艳 1郑少秋 1涂永生 2张雅洁1

作者信息

  • 1. 510182广州,广州医科大学病理教研室
  • 2. 生理教研室
  • 折叠

摘要

Abstract

Background and objective Cancer stem cells (CSCs) are responsible for multi-drug resistance in tu-mors. CD133 is a known biomarker of CSCs. hTe aim of this study is to screen for drug-resistant differentially expressed genes in CD133+and CD133-lung cancer cells and to identify novel lung tumor drug-resistant genes. Methods Magnetic activated cell sorting was used to isolate CD133+and CD133-cells from human lung cancer cell line A549, and drug-resistant microarray was used to detect drug-resistant genes in the these cells. RT-qPCR was used to examine the expression of six lung tumor drug-resistant genes in pre-and post-chemotherapeutic A549 cells. Results A total of 31 differentially expressed genes were screened by microar-ray analysis. Of these genes, 30 were upregulated and one was downregulated in CD133+cells compared with CD133-cells. Re-sults were veriifed by RT-qPCR. CYP2C19, CYP2D6, CYP2E1, GSK3α, PPARα, and PPARβ/δwere signiifcantly upregulated atfer the A549 cells were treated with 1.97μg/mL DDP or 0.61μg/mL doxorubicin for 48 h. Conclusion hTe drug resistance of lung adenosarcoma may be correlated with 31 differentially expressed genes screened by drug-resistant microarray. CYP2C19, CYP2D6, CYP2E1, GSK3α, PPARα, and PPARβ/δmight be novel lung adenosarcoma drug-resistant genes.

关键词

CD133/肺肿瘤/耐药/肿瘤耐药基因芯片

Key words

CD133/Lung neoplasms/Multi-drug resistant/Drug-resistant microarray

引用本文复制引用

王红艳,郑少秋,涂永生,张雅洁..基因芯片筛选CD133+/CD133-肺腺癌细胞中新的耐药基因[J].中国肺癌杂志,2014,(6):437-443,7.

基金项目

本研究受教育部博士点基金(No.20134423110001)、广东省自然科学基金(No.S2012010010181)、广州市科技计划项目(No.2014Y2-00171)、广州市教育系统创新学术团队项目(No.13C06)和广州市属高校科研项目(No.2012C135)资助hTis study was supported partly by the grants from Doctoral Fund of Ministry of Education of China (to Yajie ZH ANG)(No.20134423110001), Guangdong Province Natural Science Foundation(to Yajie ZHANG)(No.S2012010010181), Science and Technology Program of Guangzhou (to Yajie ZHANG)(No.2014Y2-00171), Guangzhou Municipal Education Department Innavation team grant (to Yajie ZHANG)(No.13C06), and Guangzhou City-belonged Universities Scientiifc Re-search Program (to Hongyan WANG)(No.2012C135) (to Yajie ZH ANG)

中国肺癌杂志

OA北大核心CSCDCSTPCDMEDLINE

1009-3419

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