Activation of the jun-D gene during treatment of human myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine.

Autor: Kharbanda S; Laboratory of Clinical Pharmacology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115., Huberman E, Kufe D
Jazyk: angličtina
Zdroj: Biochemical pharmacology [Biochem Pharmacol] 1993 May 25; Vol. 45 (10), pp. 2055-61.
DOI: 10.1016/0006-2952(93)90016-p
Abstrakt: The jun-D gene is a member of the c-jun family of early response genes that code for DNA binding proteins. The present studies demonstrate that 1-beta-D-arabinofuranosylcytosine (ara-C) increases jun-D expression in HL-525 myeloid leukemia cells. This induction by ara-C was maximal at 6 hr and transient. In contrast, ara-C had no detectable effect on the gene coding for the cAMP-responsive element binding protein 1. Nuclear run-on assays demonstrated that ara-C treatment is associated with an increased rate of jun-D transcription. The results also show that jun-D transcripts are stabilized at a posttranscriptional level in ara-C-treated cells. Taken together, these results demonstrate that ara-C induces expression of the jun-D gene and that this effect is regulated by transcriptional and posttranscriptional mechanisms.
Databáze: MEDLINE