Nicotine induces chromatin changes and c-Jun up-regulation in HL-60 leukemia cells

Secteur Prévention, Institut Jean-Godinot, 1 Avenue Général Koënig, 51056 Reims Cedex, France.
Oncology Reports (Impact Factor: 2.3). 01/2006; 14(6):1553-8. DOI: 10.3892/or.14.6.1553
Source: PubMed


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.

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    • "In fact, it is now well established that as a consequence of cocaine/amphetamine, alcohol or nicotine exposure, changes in the pattern of histone acetylation/deacetylation can be detected in different brain areas, and some of these changes occur in a drug-specific manner [24] [12] [15]. Furthermore, the analysis of the temporal dynamics as well as the transient or permanent nature of these changes, and the characteristics of the brain areas where they occur have allowed to link these molecular events to processes such as development of tolerance to the drug [31] and withdrawal manifestations [24] [19], among others. "
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