Suppression of nuclear ADP-ribosyltransferase activity in Ehrlich ascites tumor cells by 5-azacytidine and its analogs.

Abstract

The exposure of freshly isolated, activity growing Ehrlich ascites tumor cells to the antileukemic agent 5-azacytidine and its analogs, 5-azacytosine (but not 6-azacytosine), 5-aza-2'-deoxycytidine and, in particular, 5-fluorocytidine in the serum-free medium caused a time- and dose-dependent suppression of the nuclear ADP-ribosyltransferase activity. The azacytidine suppression was apparently dependent on the cellular activity of DNA synthesis but not related to the nuclear activity of DNA methylation, indicating the 5-azacytidine incorporation into DNA, but not drug-induced hypomethylation of DNA, being responsible for the 5-azacytidine-suppression of chromatin-bound ADP-ribosyltransferase.

• Authors: J Hoshino, J Frahm, H Kröger
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 142 Issue 2 Pg. 468-74 (Jan 30 1987) ISSN: 0006-291X [Print] United States
• PMID: 2434095 (Publication Type: Journal Article)

Chemical References

• Poly(ADP-ribose) Polymerase Inhibitors
• 5-azacytosine
• Cytosine
• DNA
• Azacitidine
• Hydroxyurea

Topics

• Animals
• Azacitidine (metabolism, pharmacology)
• Carcinoma, Ehrlich Tumor (enzymology)
• Cell Nucleus (enzymology)
• Cytosine (analogs & derivatives, pharmacology)
• DNA (metabolism)
• Female
• Hydroxyurea (pharmacology)
• Methylation
• Mice
• Mice, Inbred Strains
• Poly(ADP-ribose) Polymerase Inhibitors