汪进, 曾志雄, 黄明辉, 方宏勋, 肖培根, 韩锐, 杨梦甦. 全反式维甲酸诱导人急性早幼粒白血病HL-60细胞分化的机制J. 药学学报, 2004, 39(1): 22-28.
引用本文: 汪进, 曾志雄, 黄明辉, 方宏勋, 肖培根, 韩锐, 杨梦甦. 全反式维甲酸诱导人急性早幼粒白血病HL-60细胞分化的机制J. 药学学报, 2004, 39(1): 22-28.
WANG Jin, TZENG Chi-hung, HUANG Ming-hui, FANG Hong-xun, XIAO Pei-gen, HAN Rui, YANG Meng-su. Molecular mechanism of granulocytic differentiation of human promyelocytic leukemia HL-60 cells induced by ATRAMolecular mechanism of granulocytic differentiation of human promyelocytic leukemia HL-60 cells induced by all-trans retinoic acidJ. Acta Pharmaceutica Sinica, 2004, 39(1): 22-28.
Citation: WANG Jin, TZENG Chi-hung, HUANG Ming-hui, FANG Hong-xun, XIAO Pei-gen, HAN Rui, YANG Meng-su. Molecular mechanism of granulocytic differentiation of human promyelocytic leukemia HL-60 cells induced by ATRAMolecular mechanism of granulocytic differentiation of human promyelocytic leukemia HL-60 cells induced by all-trans retinoic acidJ. Acta Pharmaceutica Sinica, 2004, 39(1): 22-28.

全反式维甲酸诱导人急性早幼粒白血病HL-60细胞分化的机制

Molecular mechanism of granulocytic differentiation of human promyelocytic leukemia HL-60 cells induced by ATRAMolecular mechanism of granulocytic differentiation of human promyelocytic leukemia HL-60 cells induced by all-trans retinoic acid

  • 摘要: 目的研究全反式维甲酸诱导人急性早幼粒白血病HL-60细胞分化机制。方法用流式细胞仪分析维甲酸对HL-60细胞周期变化的影响,用自制的含9 984个已知基因和EST的高密度基因芯片检测HL-60细胞在维甲酸诱导作用下不同时期的基因表达变化。结果HL-60细胞在1 μmol·L-1维甲酸持续作用2,4和6 d时,流式细胞仪结果显示48%~73%细胞阻断在G0/G1期;基因表达谱分析发现,黏附分子、组织重建蛋白、转运蛋白、核蛋白体蛋白和涉及氧化酶激活途径的基因表达明显升高。结论基因表达谱的研究结果表明,维甲酸作用HL-60细胞与氧化酶激活途径及组织重建蛋白的表达相关联,并揭示了一些已知和未知功能的基因在HL-60细胞分化与细胞凋亡过程中的作用。

     

    Abstract: AimTo elucidate the molecular mechanism of granulocytic differentiation of human promyelocytic leukemia HL-60 cells induced by all-trans-retinoic acid (ATRA). MethodsFlow cytometry was used to determine the cell cycle changes of HL-60 cells upon ATRA treatment. Gene expression profiles of HL-60 cells induced by 1 μmol·L-1 ATRA were obtained by using cDNA microarrays containing 9 984 genes and expressed sequence tags (ESTs). ResultsCell cycle analysis showed that 48%-73% of cells were arrested at G1/G0 phase upon ATRA treatment; cDNA microarray results demonstrated that the expression of genes encoding adhesion molecules, tissue remodeling proteins, transporters and ribosomal proteins were up-regulated in ATRA treated of HL-60 cells. Several genes involved in oxidase activation pathway were also differentially expressed. ConclusionATRA treatment induced growth arrest and differentiation in HL-60 cells, which is associated with regulation of the oxidase activation pathway and the expression of tissue remodeling proteins.

     

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