Involvement of Arachidonic Acid Metabolites in the Transcriptional Regulation of CSF-1 Gene Expression by Tumor Necrosis Factor
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The macrophage-specific colony stimulating factor (CSF-1) regulates the hematopoietic stem cell formation of monocyte/macrophage-containing colonies (1). CSF-1 also stimulates the production of several biologic factors including prostaglandin E, plasminogen activator, interleukin 1, granulocyte-specific colony stimulating factor, interferon, myeloid colony stimulating activity and tumor necrosis factor (TNF) (2). In contrast to the known pleiotropic effects of CSF-1, the regulation of CSF-1 gene expression has not been extensively examined. Recent studies have demonstrated that phorbol esters and the granulocyte/macrophage-specific colony stimulating factor induce CSF-1 gene expression in MIA-PaCa cells, normal human monocytes, and during monocytic differentiation of human leukemia cells (3–6). Furthermore, the CSF-1 gene has been shown to be constitutively expressed in a variety of human ovarian, breast and lung carcinoma cell lines (7).
KeywordsTumor Necrosis Factor Arachidonic Acid Metabolite Lung Carcinoma Cell Line Monocytic Differentiation Tumor Necrosis Factor mRNA
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