[对伊马替尼耐药的慢性粒细胞白血病细胞系的转录组分析]
[Transcriptome Analysis of Chronic Myelogenous Leukemia Cell Line with Imatinib Resistance].
作者信息
Han Xiao, Deng Zhi-Kui, Zhang Cheng-Wan, Yu Liang, Liu Xiao-Ning
机构信息
Department of Central Laboratory, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an 223300, Jiangsu Province, China.
Department of Hematology, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an 223300, Jiangsu Province, China.
出版信息
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2021 Dec;29(6):1714-1718. doi: 10.19746/j.cnki.issn.1009-2137.2021.06.004.
OBJECTIVE
To investigate the regulation of chronic myelogenous leukemia （CML） imatinib resistant genes, in order to improve the therapeutic effect of CML imatinib resistant patients.
METHODS
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.
RESULTS
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.
CONCLUSION
CML imatinib resistance is associated with oxidative phosphorylation, during which the pathway of TGF-beta and mTOR are significantly up-regulated.
目的
研究慢性髓性白血病（CML）伊马替尼耐药基因的调控机制，以提高CML伊马替尼耐药患者的治疗效果。
方法
收集人CML细胞系K562和伊马替尼耐药的K562细胞（K562/G01），通过RNA测序获得细胞转录组。采用标准程序对测序数据进行分析。
结果
与K562细胞相比，K562/G01细胞中有464个基因发生显著变化，其中163个基因上调，301个基因下调。GO功能注释分析和KEGG通路分析结果表明，差异表达基因主要参与氧化磷酸化、蛋白质细胞器定位、核糖核蛋白复合体生物发生等生物学过程。基因集富集分析（GSEA）图显示，K562/G01中有5个基因集显著上调，包括TGF-β、mTOR和CML通路。
结论
CML伊马替尼耐药与氧化磷酸化有关，在此过程中TGF-β和mTOR通路显著上调。
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