Induction of macrophage-like differentiation of HL-60 leukemia cells by tumor necrosis factor-alpha: potential role of fos expression

Molecular Endocrinology
S P SquintoW D Davenport

Abstract

Tumor necrosis factor-alpha (TNF-alpha) is a macrophage-derived cytokine elicited during cellular responses to various microbial infections. TNF-alpha exerts direct cytotoxicity toward some tumor cells in vitro and produces hemorrhagic tumor necrosis in vivo. In human promyelocytic HL-60 leukemia cells, human recombinant TNF-alpha (rTNF-alpha) exhibits a small early proliferative effect (within 48 h), followed by marked cytostatic activity at 96 h after the addition of rTNF-alpha. Cytostasis is contiguous with an induction of cell differentiation along the monocyte/macrophage lineage. The cell proliferation effects and the induction of the differentiated phenotype are preceded by an approximate 5-fold increase in c-fos mRNA levels within 90 min after rTNF-alpha treatment of log phase HL-60 cells. Nuclear in vitro transcription assays indicate that the effect of rTNF-alpha on c-fos mRNA abundance is controlled at the transcriptional level. We have also used a postembedding immunocolloidal gold electron microscopy technique to localize and semiquantitate pp55c-fos proto-oncoprotein levels in the nucleus of both control and rTNF-alpha-treated HL-60 leukemia cells. In response to rTNF-alpha, we have observed a rapid and transient a...Continue Reading

Citations

Sep 1, 1994·Pharmacology & Therapeutics·Y Ohmori, T A Hamilton

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