Biomedical Science Letters (대한의생명과학회지)
- Volume 11 Issue 2
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- Pages.165-173
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- 2005
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- 1738-3226(pISSN)
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- 2288-7415(eISSN)
Molecular Mechanisms of 5-Azacytidine-Induced Trifluorothymidine-Resistance In Chinese Hamster V79 Cells
- Jin Kyong-Suk (Department of Biomedical Laboratory Science, Inje University) ;
- Lee Yong-Woo (Department of Biomedical Laboratory Science, Inje University)
- Published : 2005.06.01
Abstract
A potent demethylating agent, 5-Azacytidine (5-AzaC) has been widely used as in many studies on DNA methylation, regulation of gene expression, and cancer biology. The mechanisms of the demethylating activity were known to be formation of complex between DNA and DNA methyltransferase (MTase), which depletes cellular MTase activity. However, 5-AzaC can also induce hypermethylation of a transgene in a transgenic cell line, G12 cells and it was explained as a result of defense mechanisms to inactivate foreign gene(s) somehow. This finding evoked the question that whether the phenomenon of hypermethylation induced by 5-AzaC is limited to the transgene or it can be occurred in endogenous gene(s). In order to answer the question, mutagenicity test of 5-AzaC and molecular characterization of mutants obtained from the test were performed using an endogenous gene, thymidine kinase (tk) in Chinese hamster V79 cells. When V79 and V79-J3 subclone cells were treated with 1, 2.5 ,5,
Keywords
- 5-Azacytidine (5-AzaC);
- Mutagenicity;
- V79;
- Thymidine kinase(tk);
- Trifluorothymidine(TFT);
- Resistance, Methylation