Glucocorticoids (GCs) exert their effects through regulation of gene
expression after activation in the cytoplasm of the glucocorticoid receptor (GR)
encoded by NR3C1 gene. A negative feedback mechanism resulting in GR
autoregulation has been demonstrated through the binding of the activated receptor
to intragenic sequences called GRE-like elements, contained in GR gene.
The long noncoding RNA growth arrest–specific transcript 5 (GAS5) interacts with
the activated GR suppressing its transcriptional activity. The aim of this study was to
evaluate the possible role of GAS5 and NR3C1 gene expression in the antiproliferative
effect of methylprednisolone in peripheral blood mononuclear cells and
to correlate the expression with individual sensitivity to GCs. Subjects being poor responders to GCs presented
higher levels of GAS5 and NR3C1 in comparison with good responders. We suggest that abnormal levels of
GAS5 may alter GC effectiveness, probably interfering with the mechanism of GR autoregulation.
Keywords: GAS5, gene expression, glucocorticoid receptor, long noncoding RNA, methylprednisolone, NR3C1
gene, proliferation assay.
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