Matsui T, Nakao Y, Koizumi T, Katakami Y, Takahashi R, Mihara K, Sugiyama T, Fujita T
Department of Medicine, Kobe University School of Medicine, Japan.
Leuk Res. 1988;12(7):597-605. doi: 10.1016/0145-2126(88)90090-2.
The effect of prostaglandin E2 (PGE2) on the reduction of c-myc expression during the differentiation of the human leukemic cell line, HL-60, was examined. PGE2, a potent inducer of intracellular cyclic AMP (cAMP) in HL-60 cells, augmented monocyte-associated cell surface antigens induced by human gamma-interferon (IFN-gamma) or 1 alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) in these cells. The elevation of intracellular cAMP was induced dose-dependently by PGE2, but not by IFN-gamma or 1,25(OH)2D3. Changes were also seen in functional differentiation, such as, the increase of phagocytic capability and superoxide generation. PGE2 also enhanced the reduction of c-myc expression and the down-regulation of transferrin receptor by IFN-gamma or 1,25(OH)2D3, whereas PGE2 alone did not induce these phenotypic changes. These data suggest that IFN-gamma and 1,25(OH)2D3 reduce c-myc expression of HL-60 cells by a mechanism other than the augmentation of intracellular cAMP.
研究了前列腺素E2（PGE2）对人白血病细胞系HL-60分化过程中c-myc表达降低的影响。PGE2是HL-60细胞中细胞内环状AMP（cAMP）的有效诱导剂，可增强人γ-干扰素（IFN-γ）或1α,25-二羟基维生素D3（1,25(OH)2D3）诱导的这些细胞中与单核细胞相关的细胞表面抗原。PGE2可剂量依赖性地诱导细胞内cAMP升高，但IFN-γ或1,25(OH)2D3则不能。在功能分化方面也观察到了变化，如吞噬能力和超氧化物生成的增加。PGE2还增强了IFN-γ或1,25(OH)2D3对c-myc表达的降低和转铁蛋白受体的下调，而单独的PGE2不会诱导这些表型变化。这些数据表明，IFN-γ和1,25(OH)2D3通过细胞内cAMP增加以外的机制降低HL-60细胞的c-myc表达。
