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.

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

  • 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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