Abstract
Cigarette smoking is one of the most important risk factors for kidney cancer, but the molecular mechanism is poorly understood. To examine the expression change of histone H3 on lysine 27 trimethylase (H3K27me3) demethylases ubiquitously transcribed TPR gene on the X chromosome (UTX) in kidney cancer cell line 786-O after nicotine treatment, quantitative real-time-polymerase chain reaction and western blotting analysis were carried out. These results showed that nicotine can increase UTX messenger RNA and protein levels and also decrease the content of H3K27me3. The decreased content of H3K27me3 may activate specific gene expression and lead to kidney cancer. Future investigation on nicotine induced UTX expression and its epigenetic effect would deepen our understanding on nicotine toxicity and carcinogenicity.
Keywords:
Nicotine; UTX; histone demethylase; kidney cancer.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Blotting, Western
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Cell Line, Tumor
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Down-Regulation / drug effects
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Enhancer of Zeste Homolog 2 Protein
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Histone Demethylases / drug effects
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Histone Demethylases / metabolism*
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Humans
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Jumonji Domain-Containing Histone Demethylases / drug effects*
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Jumonji Domain-Containing Histone Demethylases / metabolism*
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Kidney Neoplasms / pathology
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Nicotine / pharmacology*
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Nicotinic Agonists / pharmacology*
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Nuclear Proteins / drug effects
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Nuclear Proteins / metabolism*
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Polycomb Repressive Complex 2 / metabolism
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RNA, Messenger / biosynthesis
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RNA, Messenger / genetics
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Real-Time Polymerase Chain Reaction
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Up-Regulation / drug effects
Substances
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Nicotinic Agonists
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Nuclear Proteins
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RNA, Messenger
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Nicotine
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Histone Demethylases
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Jumonji Domain-Containing Histone Demethylases
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KDM6A protein, human
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KDM6B protein, human
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EZH2 protein, human
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Enhancer of Zeste Homolog 2 Protein
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Polycomb Repressive Complex 2