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The epigenetic impact of suberohydroxamic acid and 5-Aza-2'-deoxycytidine on DNMT3B expression in myeloma cell lines differing in IL-6 expression
KS. Trtkova, P. Luzna, DW. Drozdkova, K. Cizkova, L. Janovska, J. Gursky, D. Prukova, I. Frydrych, M. Hajduch, J. Minarik
Language English Country Greece
Document type Journal Article
NLK
Free Medical Journals
from 2008 to 1 year ago
Freely Accessible Science Journals
from 2008
ProQuest Central
from 2012-01-01
Health & Medicine (ProQuest)
from 2012-01-01
- MeSH
- Decitabine * pharmacology MeSH
- DNA (Cytosine-5-)-Methyltransferases * genetics metabolism MeSH
- Epigenesis, Genetic * MeSH
- Cyclin-Dependent Kinase Inhibitor p15 genetics metabolism MeSH
- Cyclin-Dependent Kinase Inhibitor p16 genetics metabolism MeSH
- Interleukin-6 genetics metabolism MeSH
- Humans MeSH
- DNA Methylation MeSH
- Multiple Myeloma * genetics metabolism MeSH
- Cell Line, Tumor MeSH
- Tumor Suppressor Protein p53 genetics metabolism MeSH
- Cell Cycle Proteins genetics metabolism MeSH
- Gene Silencing MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
Gene inactivation of the cyclin-dependent kinase inhibitors p16INK4a, p15INK4b and p21WAF is frequently mediated by promoter gene methylation, whereas histone deacetylases (HDACs) control gene expression through their ability to deacetylate proteins. The effect of suberohydroxamic acid (SBHA) and 5-Aza-2'-deoxycytidine (Decitabine) (DAC) treatments on the transcription of CDKN2A, CDKN2B and CDKN1A genes, and their effects on molecular biological behavior were examined in two myeloma cell lines, RPMI8226 and U266, which differ in p53-functionality and IL-6 expression. In both tested myeloma cell lines, a non-methylated state of the CDKN2B gene promoter region was detected with normal gene expression, and the same level of p15INK4b protein was detected by immunocytochemical staining. Furthermore, in myeloma cells treated with SBHA and DAC alone, the expression of both p15INK4b and p21WAF was significantly upregulated in RPMI8226 cells (p53-functional, without IL-6 expression), whereas in the U266 cell line (p53 deleted, expressing IL-6) only p21WAF expression was significantly increased. Moreover, the analysis revealed that treatment with DAC induced DNMT3B enhancement in U266 cells. In conclusion, in myeloma cells with IL-6 expression, significantly increased DNMT3B expression indicated the tumorigenic consequences of 5-Aza-2'deoxycytidine treatment, which requires careful use in diseases involving epigenetic dysregulation, such as multiple myeloma (MM).
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- $a Gene inactivation of the cyclin-dependent kinase inhibitors p16INK4a, p15INK4b and p21WAF is frequently mediated by promoter gene methylation, whereas histone deacetylases (HDACs) control gene expression through their ability to deacetylate proteins. The effect of suberohydroxamic acid (SBHA) and 5-Aza-2'-deoxycytidine (Decitabine) (DAC) treatments on the transcription of CDKN2A, CDKN2B and CDKN1A genes, and their effects on molecular biological behavior were examined in two myeloma cell lines, RPMI8226 and U266, which differ in p53-functionality and IL-6 expression. In both tested myeloma cell lines, a non-methylated state of the CDKN2B gene promoter region was detected with normal gene expression, and the same level of p15INK4b protein was detected by immunocytochemical staining. Furthermore, in myeloma cells treated with SBHA and DAC alone, the expression of both p15INK4b and p21WAF was significantly upregulated in RPMI8226 cells (p53-functional, without IL-6 expression), whereas in the U266 cell line (p53 deleted, expressing IL-6) only p21WAF expression was significantly increased. Moreover, the analysis revealed that treatment with DAC induced DNMT3B enhancement in U266 cells. In conclusion, in myeloma cells with IL-6 expression, significantly increased DNMT3B expression indicated the tumorigenic consequences of 5-Aza-2'deoxycytidine treatment, which requires careful use in diseases involving epigenetic dysregulation, such as multiple myeloma (MM).
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