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Regulation of jun-B gene expression by 1-beta-D-arabinofuranosyl- cytosine in human myeloid leukemia cells

R Datta, S Kharbanda and D Kufe

Laboratory of Clinical Pharmacology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115.

The jun-B gene is a member of the jun family of immediate early response genes that regulate cellular responses to growth factors. The present studies have examined the effects of 1-beta-D- arabinofuranosylcytosine (ara-C) on jun-B expression in human KG-1 myeloid leukemia cells. The results demonstrate that ara-C increases jun-B mRNA levels. The level of jun-B transcripts was maximal after 12 hr of exposure to 10(-5) M ara-C and persisted through 72 hr. Nuclear run-on assays demonstrated that ara-C treatment is associated with an increased rate of jun-B gene transcription. The results also demonstrate that ara-C-induced jun-B mRNA levels are regulated by a posttranscriptional mechanism. The level of jun-B transcripts in ara-C- treated cells was superinduced by inhibition of protein synthesis. Moreover, cycloheximide prolonged the half-life of ara-C-induced jun-B transcripts. These results, thus, demonstrate that ara-C induces expression of the jun-B gene in KG-1 cells and that this effect is mediated by transcriptional and posttranscriptional mechanisms.

Volume 38, Issue 4, pp. 435-439, 10/01/1990
Copyright © 1990 by American Society for Pharmacology and Experimental Therapeutics




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