[急性髓系白血病中阿糖胞苷耐药的机制]
[Mechanism of in Cytarabine Resistance in Acute Myeloid Leukemia].
作者信息
Feng Jia-Wei, Yu Hong-Juan
机构信息
Department of Hematology, Southern University of Science and Technology Hospital, Shenzhen 518055, Guangdong Province, China.
出版信息
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2025 Jun;33(3):648-652. doi: 10.19746/j.cnki.issn.1009-2137.2025.03.004.
OBJECTIVE
To investigate the role of in the cytarabine (Ara-C) resistance mechanism of acute myeloid leukemia (AML) cells.
METHODS
Overexpression and silencing of gene in THP-1 cells were used to observe whether the sensitivity of THP-1 cells to Ara-C was altered. RT-PCR was used to detect the changes in mRNA expression of related genes during Ara-C transport or metabolism. Western blot and RT-PCR were used to detect SAMHD1 expression after regulating expression in Ara-C treated cells. Co-IP technology was used to detect the interaction between Cyclin L2, , and SAMHD1.
RESULTS
Overexpression of decreased Ara-C sensitivity in THP-1 cells while silencing increased it. Overexpression and silencing of did not affect Ara-C transport or metabolic gene expression. Overexpression of could increase the expression of SAMHD1 protein in cells, while silencing reduced SAMHD1 expression. Cyclin L2 interacted with and SAMHD1 in THP-1 cells.
CONCLUSION
is involved in Ara-C resistance in AML cells, and its mechanism may be related to increased expression of SAMHD1 by interacting with Cyclin L2.
目的
探讨[具体基因名称未给出]在急性髓系白血病（AML）细胞阿糖胞苷（Ara-C）耐药机制中的作用。
方法
利用THP-1细胞中[具体基因名称未给出]基因的过表达和沉默来观察THP-1细胞对Ara-C的敏感性是否改变。采用RT-PCR检测Ara-C转运或代谢过程中相关基因mRNA表达的变化。在Ara-C处理的细胞中调节[具体基因名称未给出]表达后，用蛋白质免疫印迹法（Western blot）和RT-PCR检测SAMHD1的表达。采用免疫共沉淀（Co-IP）技术检测细胞周期蛋白L2（Cyclin L2）、[具体基因名称未给出]和SAMHD1之间的相互作用。
结果
[具体基因名称未给出]的过表达降低了THP-1细胞对Ara-C的敏感性，而[具体基因名称未给出]的沉默则增加了其敏感性。[具体基因名称未给出]的过表达和沉默不影响Ara-C转运或代谢基因的表达。[具体基因名称未给出]的过表达可增加细胞中SAMHD1蛋白的表达，而[具体基因名称未给出]的沉默则降低SAMHD1的表达。在THP-1细胞中，细胞周期蛋白L2与[具体基因名称未给出]和SAMHD1相互作用。
结论
[具体基因名称未给出]参与AML细胞对Ara-C的耐药，其机制可能与通过与细胞周期蛋白L2相互作用增加SAMHD1的表达有关。
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