| 王永生,丁晶晶,苗立云.人肺腺癌吉非替尼获得性耐药株H1975细胞与敏感株PC9细胞miRNA谱表达差异[J].中国肿瘤,2013,22(9):743-747. |
| 人肺腺癌吉非替尼获得性耐药株H1975细胞与敏感株PC9细胞miRNA谱表达差异 |
| Difference of microRNA Expression Profiles between EGFR Double Mutations Human Lung Adenocarcinoma Cell Line H1975 and EGFR Single Mutation Cell Line PC9 |
| 投稿时间：2012-12-20 |
| DOI：10.11735/j.issn.1004-0242.2013.09.A015 |
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| 中文关键词: 肺癌 耐药 微小RNA 基因芯片 酪氨酸激酶抑制剂 |
| 英文关键词:lung cancer drug resistance micro RNAs microarray analysis tyrosine kinase inhibitor TKI |
| 基金项目: |
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| 中文摘要: |
| 摘 要：［目的］分析人肺腺癌吉非替尼耐药细胞株H1975（epidermal growth factor receptor，EGFR基因双突变）和人肺腺癌吉非替尼敏感细胞株PC9（EGFR单突变）细胞株微小RNA(microRNA，miRNA)表达谱的差异。［方法］ 用Agilent human miRNA芯片分别检测H1975细胞与PC9细胞株的miRNA表达谱，Agilent Feature Extraction软件分析并筛选表达差异达5倍以上的miRNA，生物学软件分析表达差异miRNA的可能靶基因。实时定量PCR(qRT-PCR)验证miRNA芯片结果。［结果］与PC9细胞相比，H1975细胞株中22个miRNA表达上调>5倍，24个miRNA表达下调>5倍。qRT-PCR结果验证了芯片的结果(上调的如hsa-miR-489，hsa-miR-210和hsa-miR-21等；下调的如hsa-miR-205，hsa-miR-200c和hsa-miR-155等)，同时发现，其中33个异常表达的miRNA有潜在的靶基因，靶基因超过100个的有24个miRNA。［结论］H1975吉非替尼耐药与miRNA谱异常表达有关，miRNA可能通过调控靶基因而参与EGFR-TKI的获得性耐药。 |
| 英文摘要: |
| Abstract:［Purpose］ To differentiate microRNA(miRNAs) profiles in EGFR double mutations cell line-H1975 versus EGFR single mutation cell line-PC9. ［Methods］ The microRNA(miRNA) expression profiles of H1975 and PC9 cells were analyzed by Agilent human miRNA microarray. The Agilent Feature Extraction software was used to analyze the differential expression of miRNA，and bioinformatics software was used to predict the potential target genes of differentially expressed miRNAs. RT-PCR was used to confirm the result of microRNA microarray. ［Results］ Twenty-two miRNAs were up-regulated and 24 down-regulated over 5 folds in H1975 compared with PC9 cell line. RT-PCR confirmed the result of miRNA microarray（hsa-miR-489，hsa-miR-21 and hsa-miR-21，et al. were up-regulated；hsa-miR-205，hsa-miR-200c and hsa-miR-155，et al. were down-regulated）. The bioinformatics analysis revealed that 33miRNAs had their potential target genes，and 24 of which had the potential target genes over 100. ［Conclusion］ The acquired resistance to EGFR-TKI might be correlated to de-regulated miRNAs. |
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