[Transcriptome Analysis of Chronic Myelogenous Leukemia Cell Line with Imatinib Resistance]

To investigate the regulation of chronic myelogenous leukemia （CML） imatinib resistant genes, in order to improve the therapeutic effect of CML imatinib resistant patients.The human CML cell line K562 and imatinib-resistant K562 cells (K562/G01) were collected, and transcriptome of the cells were achieved by RNA-seq. The sequencing data were analyzed by using standard procedures.Compared with K562 cells, 464 genes were significantly changed in K562/G01 cells, including 163 up-regulated and 301 down-regulated genes. The GO function annotation analysis and KEGG pathway analysis results showed that the differentially expressed genes were mainly involved in biological processes such as oxidative phosphorylation, localization to protein organelle, ribonucleoprotein complex biogenesis and so on. Gene Set Enrichment Analysis (GSEA) plots showed that 5 gene-sets were up-regulated in K562/G01 significantly, including the pathway of TGF-beta, mTOR and CML.CML imatinib resistance is associated with oxidative phosphorylation, during which the pathway of TGF-beta and mTOR are significantly up-regulated.慢性粒细胞白血病耐伊马替尼细胞系的转录组分析.探讨调控慢性粒细胞白血病（CML）耐伊马替尼的基因，以提高CML耐伊马替尼患者的治疗效果.选取伊马替尼敏感细胞系K562和耐药细胞系K562/G01，采用RNA-seq方法获得对应细胞的转录组，并进行标准生物信息学分析.相较于K562细胞，耐伊马替尼细胞K562/G01转录组中共有464个表达显著变化的基因，其中163个基因表达上调，301个基因表达下调。GO功能注释分析和KEGG通路的富集分析结果显示，差异基因主要集中在氧化磷酸化、蛋白细胞器定位、核糖核蛋白复合体的生物发生等生物学过程。GSEA基因富集分析表明，有5个基因集在K562/G01中被显著的上调，如TGF-beta信号通路、mTOR信号通路、慢性粒细胞白血病相关信号通路等.CML细胞伊马替尼耐药与细胞中氧化磷酸化过程有关，在耐药过程中TGF-beta信号通路、mTOR信号通路发生显著上调.