Suppression of nuclear ADP-ribosyltransferase activity in Ehrlich ascites tumor cells by 5-azacytidine and its analogs.
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.
D000818:Animals; D001374:Azacitidine / Q000378:metabolism / Q000494:pharmacology*; D002286:Carcinoma, Ehrlich Tumor / Q000201:enzymology*; D002467:Cell Nucleus / Q000201:enzymology*; D003596:Cytosine / Q000031:analogs & derivatives / Q000494:pharmacology; D004247:DNA / Q000378:metabolism; D005260:Female; D006918:Hydroxyurea / Q000494:pharmacology; D008745:Methylation; D051379:Mice; D008815:Mice, Inbred Strains; D000067856:Poly(ADP-ribose) Polymerase Inhibitors
D000067856:Poly(ADP-ribose) Polymerase Inhibitors; C039854:5-azacytosine; D003596:Cytosine; D004247:DNA; D001374:Azacitidine; D006918:Hydroxyurea