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*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

11 Citations (Scopus)


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 languageEnglish
Pages (from-to)1553-1558
Number of pages6
JournalOncology Reports
Issue number6
Publication statusPublished - Dec 2005
Externally publishedYes


  • Chromatin
  • HL-60 cells
  • Histone acetylation
  • Image analysis
  • Nicotine
  • Transcription factors


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