Transient down-regulation of c-myc protooncogene expression by the alkaloid nicotine in human promyelocytic HL-60 cells.

Human promyelocytic leukemia cells (HL-60) acquire monocytic biochemical characteristics when exposed to the alkaloid nicotine. We report herein that the nicotine-induced phenotype change is accompanied by the transient reduced expression of mRNA for the protooncogene c-myc. The suppressive effect of nicotine on c-myc mRNA levels is not reversed by the addition of ADP-ribosyl transferase inhibitor, 3-aminobenzamide.