Microarray analysis and establishment of drug screening platform using 5-fluorouracil resistance HCT116 colon cancer cells

Genomic Medicine, Biomarkers, and Health Sciences Pub Date : 2012-03-01 DOI:10.1016/j.gmbhs.2012.04.001

Ailun Heather Tseng , Feng-Hsiang Chung , Hoong-Chien Lee , Li-Ching Wu , Chang-Han Chen , Li-Jen Su

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引用次数: 1

Abstract

A systemic approach was used to identify the possible mechanisms underlying the development of 5-fluorouracil (5FU)-induced resistance on HCT116 colon cancer cells. From microarray analysis, HCT116 high-dose 5FU-resistant subclones showed differential gene expression compared to HCT116-sensitive clones. According to gene ontology, and Kyoto Encyclopedia of Genes and Genomes pathways, the up-regulated genes were related to cell death and lupus erythematosus, respectively. On the other hand, the down-regulated genes were related to cell division or DNA replication. Connectivity map (cMAP) analysis revealed that the molecular drugs, such as antiasthmatic or antiallergy agents that have negative correlations with cMAP score, may have beneficial effect for the resistant subclones. Our findings suggested that the feasibility of cMAP combining microarray gene expression profile may help identify a potential drug that possibly will reverse the effect of 5FU-induced resistance.

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5-氟尿嘧啶耐药HCT116结肠癌细胞的芯片分析及药物筛选平台的建立

采用系统方法确定5-氟尿嘧啶(5FU)诱导HCT116结肠癌细胞耐药发生的可能机制。微阵列分析显示，与HCT116敏感克隆相比，HCT116高剂量5fu耐药亚克隆的基因表达存在差异。根据基因本体论和京都基因与基因组途径百科，上调的基因分别与细胞死亡和红斑狼疮有关。另一方面，下调的基因与细胞分裂或DNA复制有关。连通性图(cMAP)分析显示，与cMAP评分呈负相关的分子药物，如平喘药或抗过敏药，可能对耐药亚克隆有有益作用。我们的研究结果表明，cMAP结合微阵列基因表达谱的可行性可能有助于确定一种可能逆转5fu诱导的耐药效应的潜在药物。

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Genomic Medicine, Biomarkers, and Health Sciences

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