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Dual Effect of Taxifolin on ZEB2 Cancer Signaling in HepG2 Cells
Z. Dostal, M. Sebera, J. Srovnal, K. Staffova, M. Modriansky
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články
Grantová podpora
RVO 61989592
Ministry of Education of the Czech Republic
IGA_LF_2020_022
Palacký University
NLK
Directory of Open Access Journals
od 1997
Free Medical Journals
od 1997
PubMed Central
od 2001
Europe PubMed Central
od 2001
ProQuest Central
od 1997-01-01
Open Access Digital Library
od 1997-01-01
Medline Complete (EBSCOhost)
od 2009-03-01
Health & Medicine (ProQuest)
od 1997-01-01
- MeSH
- apoptóza účinky léků MeSH
- buňky Hep G2 metabolismus MeSH
- epitelo-mezenchymální tranzice genetika MeSH
- exprese genu účinky léků genetika MeSH
- hepatocyty účinky léků metabolismus MeSH
- lidé MeSH
- mikro RNA účinky léků genetika MeSH
- pohyb buněk účinky léků MeSH
- polyfenoly farmakologie MeSH
- primární buněčná kultura MeSH
- proliferace buněk účinky léků MeSH
- quercetin analogy a deriváty metabolismus farmakologie MeSH
- regulace genové exprese u nádorů účinky léků MeSH
- signální transdukce genetika MeSH
- transkripční faktor Zeb2 účinky léků metabolismus MeSH
- transkriptom účinky léků genetika MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
Polyphenols, secondary metabolites of plants, exhibit different anti-cancer and cytoprotective properties such as anti-radical, anti-angiogenic, anti-inflammation, or cardioprotective. Some of these activities could be linked to modulation of miRNAs expression. MiRNAs play an important role in posttranscriptional regulation of their target genes that could be important within cell signalling or preservation of cell homeostasis, e.g., cell survival/apoptosis. We evaluated the influence of a non-toxic concentration of taxifolin and quercetin on the expression of majority human miRNAs via Affymetrix GeneChip™ miRNA 3.0 Array. For the evaluation we used two cell models corresponding to liver tissue, Hep G2 and primary human hepatocytes. The array analysis identified four miRNAs, miR-153, miR-204, miR-211, and miR-377-3p, with reduced expression after taxifolin treatment. All of these miRNAs are linked to modulation of ZEB2 expression in various models. Indeed, ZEB2 protein displayed upregulation after taxifolin treatment in a dose dependent manner. However, the modulation did not lead to epithelial mesenchymal transition. Our data show that taxifolin inhibits Akt phosphorylation, thereby diminishing ZEB2 signalling that could trigger carcinogenesis. We conclude that biological activity of taxifolin may have ambiguous or even contradictory outcomes because of non-specific effect on the cell.
Citace poskytuje Crossref.org
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- $a Polyphenols, secondary metabolites of plants, exhibit different anti-cancer and cytoprotective properties such as anti-radical, anti-angiogenic, anti-inflammation, or cardioprotective. Some of these activities could be linked to modulation of miRNAs expression. MiRNAs play an important role in posttranscriptional regulation of their target genes that could be important within cell signalling or preservation of cell homeostasis, e.g., cell survival/apoptosis. We evaluated the influence of a non-toxic concentration of taxifolin and quercetin on the expression of majority human miRNAs via Affymetrix GeneChip™ miRNA 3.0 Array. For the evaluation we used two cell models corresponding to liver tissue, Hep G2 and primary human hepatocytes. The array analysis identified four miRNAs, miR-153, miR-204, miR-211, and miR-377-3p, with reduced expression after taxifolin treatment. All of these miRNAs are linked to modulation of ZEB2 expression in various models. Indeed, ZEB2 protein displayed upregulation after taxifolin treatment in a dose dependent manner. However, the modulation did not lead to epithelial mesenchymal transition. Our data show that taxifolin inhibits Akt phosphorylation, thereby diminishing ZEB2 signalling that could trigger carcinogenesis. We conclude that biological activity of taxifolin may have ambiguous or even contradictory outcomes because of non-specific effect on the cell.
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