Fraser J K, Guerra J J, Nguyen C Y, Indes J E, Gasson J C, Nimer S D
Department of Medicine, UCLA School of Medicine 90024.
Mol Cell Biol. 1994 Mar;14(3):2213-21. doi: 10.1128/mcb.14.3.2213-2221.1994.
Human granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulates the proliferation and maturation of normal myeloid progenitor cells and can also stimulate the growth of acute myelogenous leukemia (AML) blasts. GM-CSF is not normally produced by resting cells but is expressed by a variety of activated cells including T lymphocytes, macrophages, and certain cytokine-stimulated fibroblasts and endothelial cells. Production of GM-CSF by cultured AML cells has been demonstrated, and GM-CSF expression by normal myeloid progenitors has been postulated to play a role in myelopoiesis. We have investigated the regulation of expression of GM-CSF in AML cell lines, and our results demonstrate the presence of a strong constitutive promoter element contained within 53 bp upstream of the cap site. We have also identified a negative regulatory element located immediately upstream of the positive regulatory element (within 69 bp of the cap site) that is active in AML cell lines but not T cells or K562 CML cells. Competition transfection and mobility shift studies demonstrate that this activity correlates with binding of a 45-kDa protein.
人粒细胞-巨噬细胞集落刺激因子(GM-CSF)可刺激正常髓系祖细胞的增殖和成熟,也能刺激急性髓性白血病(AML)原始细胞的生长。GM-CSF通常不由静止细胞产生,而是由多种活化细胞表达,包括T淋巴细胞、巨噬细胞以及某些细胞因子刺激的成纤维细胞和内皮细胞。已证实培养的AML细胞可产生GM-CSF,并且推测正常髓系祖细胞的GM-CSF表达在骨髓生成中起作用。我们研究了AML细胞系中GM-CSF表达的调控,我们的结果表明在帽位点上游53 bp内存在一个强大的组成型启动子元件。我们还鉴定出一个负调控元件,位于正调控元件的紧邻上游(帽位点69 bp内),该元件在AML细胞系中具有活性,但在T细胞或K562慢性粒细胞白血病细胞中无活性。竞争转染和迁移率变动研究表明,这种活性与一种45 kDa蛋白的结合相关。