VE-statin/Egfl7基因沉默对恶性胶质瘤细胞U251基因表达谱的影响  

Effects of VE-statin/Egfl7 gene silencing on gene expression profiles of malignant glioma cell U251

作　　者：黄纯海[1] 田志[1] 万一[1] 张晶晶[1] 

机构地区：[1]吉首大学第一附属医院神经外科,湖南吉首416000

出　　处：《中华临床医师杂志（电子版）》2013年第17期90-94,共5页Chinese Journal of Clinicians(Electronic Edition)

基　　金：湖南省教育厅优秀青年项目(11B100);湖南省卫生厅科研基金(B2010-134)

摘　　要：目的探讨VE-statin/Egfl7基因在恶性胶质瘤中表达的分子调控机制。方法用小RNA干扰技术沉默VE-statin/Egfl7基因在人恶性胶质瘤U251细胞中的表达,然后用基因表达谱芯片研究VE-statin/Egfl7基因沉默前后该细胞基因表达谱的变化,进行生物信息学分析。并选取两条差异表达基因用实时荧光定量PCR进行验证。结果通过RNA干扰技术明显抑制了VE-statin/Egfl7基因在U251细胞中的表达。基因表达芯片检测结果发现与对照组相比,实验组下调基因有141条,包括未知功能基因7条,已知功能基因134条;上调的基因有130条,包括未知功能基因3条,已知功能基因127条。通过生物信息学分析发现这些基因主要与细胞增殖分化、凋亡及细胞外基质黏附等生物学功能密切相关,涉及的主要信号通路包括表皮生长因子受体ERBB家族信号、细胞存活信号及整合素ανβ3信号。结论 VE-statin/Egfl7在恶性胶质瘤中的分子调控机制可能通过PI3K/Akt和Ras/MAPK两条信号转导通路实现,为进一步研究VE-statin/Egfl7的功能和分子机制提供了新的线索。Objective To explore the molecular mechanism of VE-statin/Egfl7 gene expression in malignant gliomas. Methods The expression of VE-statin/Egfl7 gene was silenced in human malignant glioma U251 by small interfering RNA, then the changes of gene expression in the cell were studied by gene expression microarray before and after VE-statin/Egfl7 gene silencing. Bioinformafics methods were introduced to analyse the data. Two differentially expressed genes were validated by real-time fluorescence quantitative PCR. Results The expression of VE-stafin/Egfl7 gene was significantly inhibited in U251 cells by RNA interference. Gene expression mieroarray results showed that there were 141 down-regulated genes, including 7 unknown function genes and 134 known function genes, and there were 130 upregulated genes, including 3 unknown function genes, and 127 known function genes in the experimental group compared those of the control group. Bioinformatic analysis revealed that these genes were closely related to the biological functions including cell proliferation, differentiation, apoptosis and extracellular matrix adhesion, and the major signaling pathways involved of these genes were epidermal growth factor receptor signaling ERBB family, cell survival and integrin signaling ave3 signal. Conclusion Molecular regulatory mechanism of VE-statin/Egfl7 in malignant gliomasmay be put into effect through PI3K/Akt and Ras/MAPK signal transduction pathways, and the findings provide new clues to the further study of the function and molecular mechanism of VE-statin/Egfl7.

关 键 词：基因沉默 基因表达谱 类表皮生长因子域7 恶性胶质瘤 

分 类 号：R739.4[医药卫生—肿瘤]