Abstract
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.
Original language | English |
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Pages (from-to) | 1553-1558 |
Number of pages | 6 |
Journal | Oncology Reports |
Volume | 14 |
Issue number | 6 |
DOIs | |
Publication status | Published - Dec 2005 |
Externally published | Yes |
Keywords
- Chromatin
- HL-60 cells
- Histone acetylation
- Image analysis
- Nicotine
- Transcription factors