Insulin receptor substrate 1 gene expression is strongly up-regulated by HSPB8 silencing in U87 glioma cells
The aim of the present investigation was to study the expression of genes encoding IRS1 (insulin receptor substrate 1) and some other functionally active proteins in U87 glioma cells under silencing of polyfunctional chaperone HSPB8 for evaluation of the possible significance of this protein in inte...
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Veröffentlicht in: | Endocrine regulations (Bratislava) 2020-10, Vol.54 (4), p.231-243 |
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Sprache: | eng |
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Zusammenfassung: | The aim of the present investigation was to study the expression of genes encoding IRS1 (insulin receptor substrate 1) and some other functionally active proteins in U87 glioma cells under silencing of polyfunctional chaperone HSPB8 for evaluation of the possible significance of this protein in intergenic interactions.
Silencing of HSPB8 mRNA was introduced by HSPB8 specific siRNA. The expression level of
,
,
,
,
,
,
,
,
,
, and
genes was studied in U87 glioma cells by quantitative polymerase chain reaction.
It was shown that silencing of HSPB8 mRNA by specific to HSPB8 siRNA led to a strong down-regulation of this mRNA and significant modification of the expression of IRS1 and many other genes in glioma cells: strong up-regulated of
,
, and
and down-regulated of
,
,
,
, and
gene expressions. At the same time, no significant changes were detected in the expression of
gene in glioma cells treated by siRNA, specific to HSPB8. Moreover, the silencing of HSPB8 mRNA enhanced the glioma cells proliferation rate.
Results of this investigation demonstrated that silencing of HSPB8 mRNA affected the expression of
gene as well as many other genes encoding tumor growth related proteins. It is possible that the dysregulation of most of the studied genes in glioma cells after silencing of HSPB8 is reflected by a complex of intergenic interactions and that this polyfunctional chaperone is an important factor for the stability of genome function and regulatory mechanisms contributing to the tumorigenesis control. |
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ISSN: | 1336-0329 1210-0668 1336-0329 |
DOI: | 10.2478/enr-2020-0026 |