Nicotine induces chromatin changes and c-Jun up-regulation in HL-60 leukemia cells
- Emilie Landais
- Victoria El-Khoury
- Alain Prevost
- Jean Dufer
- Françoise Liautaud-Roger
Published online on: Thursday, December 1, 2005
Although nicotine has been implicated as a potential factor in the pathogenesis of human cancer, its mechanisms of action regarding cancer development remain largely unknown. HL-60 cells were used to investigate the effects of a short-term treatment with nicotine at concentrations found in the blood of smokers. The findings show that nicotine induces chromatin decondensation, histone H3 acetylation and up-regulation of the c-Jun transcription factor mRNA. This increase is inhibited by mecamylamine, a nicotinic receptor antagonist, suggesting that nicotine alters cellular function directly via nicotinic acetylcholine receptors and may then play a role in cell physiology and tumor promotion.