Wang Jin, Tzeng Chi-hung, Huang Ming-hui, Fang Hong-xun, Xiao Pei-gen, Han Rui, Yang Meng-su
Applied Research Center for Genomic Technology, Department of Biology and Chemistry, City University of Hong Kong, 83 Tat Chee Avenue, Hong Kong, China.
Yao Xue Xue Bao. 2004 Jan;39(1):22-8.
To elucidate the molecular mechanism of granulocytic differentiation of human promyelocytic leukemia HL-60 cells induced by all-trans-retinoic acid (ATRA).
Flow 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 mumol.L-1 ATRA were obtained by using cDNA microarrays containing 9,984 genes and expressed sequence tags (ESTs).
Cell 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.
ATRA 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.
阐明全反式维甲酸（ATRA）诱导人早幼粒细胞白血病HL-60细胞粒系分化的分子机制。
采用流式细胞术检测ATRA处理后HL-60细胞的细胞周期变化。利用包含9984个基因和表达序列标签（EST）的cDNA微阵列获得1μmol.L-1 ATRA诱导的HL-60细胞的基因表达谱。
细胞周期分析显示，ATRA处理后48%-73%的细胞停滞于G1/G0期；cDNA微阵列结果表明，在经ATRA处理的HL-60细胞中，编码黏附分子、组织重塑蛋白、转运蛋白和核糖体蛋白的基因表达上调。一些参与氧化酶激活途径的基因也存在差异表达。
ATRA处理诱导HL-60细胞生长停滞和分化，这与氧化酶激活途径的调节及组织重塑蛋白的表达有关。
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