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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
Jazyk angličtina Země Řecko
Typ dokumentu časopisecké články
NLK
Free Medical Journals
od 2008 do Před 1 rokem
Freely Accessible Science Journals
od 2008
ProQuest Central
od 2012-01-01
Health & Medicine (ProQuest)
od 2012-01-01
PubMed
36043519
DOI
10.3892/mmr.2022.12837
Knihovny.cz E-zdroje
- MeSH
- decitabin * farmakologie MeSH
- DNA-(cytosin-5-)methyltransferasa * genetika metabolismus MeSH
- epigeneze genetická * MeSH
- inhibitor p15 cyklin-dependentní kinasy genetika metabolismus MeSH
- inhibitor p16 cyklin-dependentní kinasy genetika metabolismus MeSH
- interleukin-6 genetika metabolismus MeSH
- lidé MeSH
- metylace DNA MeSH
- mnohočetný myelom * genetika metabolismus MeSH
- nádorové buněčné linie MeSH
- nádorový supresorový protein p53 genetika metabolismus MeSH
- proteiny buněčného cyklu genetika metabolismus MeSH
- umlčování genů MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články 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 Trtkova, Katerina Smesny $u Department of Clinical and Molecular Pathology, Faculty of Medicine and Dentistry, Palacky University Olomouc, 777 15 Olomouc, Czech Republic
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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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