欢迎访问《现代生物医学进展》编辑部！

目的：探讨两种酪氨酸激酶抑制剂（TKIs）处理K562 细胞的基因表达谱变化，为认识慢性粒细胞白血病（CML）的发病机制、耐药机制提供新的思路，同时也为治疗寻找潜在重要靶标分子。方法：利用GEO 数据库下载慢性粒细胞细胞系（K562）基因表达芯片数据，通过差异基因的筛选，趋势分析、GO 分析，信号通路分析，最后获得的重要差异表达核心基因，并建立相互作用网络。结果：获得显著表达差异基因1000，通过趋势分析、功能富集分析及信号通路分析提示主要涉及到代谢途径、细胞凋亡、癌症的途径、细胞周期、p53 信号通路。相互作用网络分析及同表达相互作用网络分析，得到重要的核心节点基因：AK2、ADSL、PKLR、 PKM、SHMT2、ATIC、LDHA、ENO1、CTH、GOT1；YARS、CYP3A5、CTH、GYPA、ALAS2、MTHFD2、BLVRB、GUK1、CTSH、LMO2。结论：利用生物信息学的方法，分析慢性粒细胞白血病细胞基因芯片得到参与不同TKIs 处理K562细胞的重要的细胞功能及信号通路主要涉及代谢通路及增殖凋亡信号途径，并且寻找到核心节点基因，为认识K562 的耐药机制及治疗靶点提供新的思路。

英文摘要:

Objective:To screen different express genes of K562 cells treated by two kinds of TKIs by using the GEO database and explore the bioinformatics information, so as to provide the new molecular markers for treatment and resistance.Methods:The microarray data were collected from GEO database. SAMwas used to find the DEGs, and then all DEGs were analyzed by STC, GO and Pathway analysis, finally created the gene signal network and gene coexpression networks.Results:There were 1000 DEGs, moreover the main results of GO and pathway analysis of DEGs were Metabolic pathways, Apoptosis, Pathways in cancer, Cell cycle, p53 signaling pathway. At last, we found the top 20 core of node genes, there were AK2, ADSL, PKLR, PKM, SHMT2, ATIC, LDHA, ENO1, CTH,GOT1, YARS, CYP3A5, CTH, GYPA, ALAS2, MTHFD2, BLVRB, GUK1, CTSH, LMO2.Conclusion:By using bioinformatics methods, we analyzed the gene chips of K562，which helped us to understand the mechanism during TKI resistance and provided new potential treatment of targeted genes.

查看全文查看/发表评论下载PDF阅读器

关闭