建立具有人源KIT N822K基因过表达的FDC-P1小鼠细胞系。
Establishment of a FDC-P1 Murine Cell Line with Human KIT N822K Gene Overexpression.
作者信息
Vagapova E R, Lebedev T D, Popenko V I, Leonova O G, Spirin P V, Prassolov V S
机构信息
Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991 Russia.
出版信息
Acta Naturae. 2020 Jan-Mar;12(1):51-55. doi: 10.32607/actanaturae.10938.
The mechanism of resistance of leukemia cells to chemotherapeutic drugs remains poorly understood. New model systems for studying the processes of malignant transformation of hematopoietic cells are needed. Based on cytokine-dependent murine acute myeloid leukemia (AML) FDC-P1 cells, we generated a new cell line with ectopic expression of the gene encoding mutant human receptor tyrosine kinase (N822K). We investigated the role played by overexpression of the mutant in the survival of leukemia cells and their sensitivity to therapeutic drugs. We also generated a co-culture system consisting of FDC-P1 murine leukemia cells and a HS-5 human stromal cell line. Our data can be used for a further comprehensive analysis of the role of N822K mutation in the cellular response to anti-leukemic drugs, growth factors, and cytokines. These data are of interest in the development of new effective therapeutic approaches to the treatment of acute leukemia.
白血病细胞对化疗药物的耐药机制仍未得到充分了解。需要新的模型系统来研究造血细胞恶性转化的过程。基于细胞因子依赖性小鼠急性髓系白血病（AML）FDC-P1细胞，我们构建了一个新的细胞系，该细胞系异位表达编码突变型人受体酪氨酸激酶（N822K）的基因。我们研究了突变体的过表达在白血病细胞存活及其对治疗药物敏感性中所起的作用。我们还构建了一个由FDC-P1小鼠白血病细胞和HS-5人基质细胞系组成的共培养系统。我们的数据可用于进一步全面分析N822K突变在细胞对抗白血病药物、生长因子和细胞因子反应中的作用。这些数据对于开发治疗急性白血病的新有效治疗方法具有重要意义。
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