Nicotine induces chromatin changes and c-Jun up-regulation in HL-60 leukemia cells
| Autor: | A. Prevost, Emilie Landais, Jean Dufer, Victoria El-Khoury, Françoise Liautaud-Roger |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Nicotine
Cancer Research Time Factors Proto-Oncogene Proteins c-jun Immunoblotting Gene Expression HL-60 Cells Nicotinic Antagonists Mecamylamine Histones Leukemia Promyelocytic Acute medicine Humans RNA Messenger Histone H3 acetylation Transcription factor Acetylcholine receptor Cell Nucleus Dose-Response Relationship Drug biology Reverse Transcriptase Polymerase Chain Reaction Acetylation General Medicine Chromatin Up-Regulation Cell biology Histone Nicotinic agonist Oncology biology.protein Cancer research Proto-Oncogene Proteins c-fos medicine.drug |
| Zdroj: | Oncology Reports. |
| ISSN: | 1791-2431 1021-335X |
| DOI: | 10.3892/or.14.6.1553 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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