Glucocorticoid receptor function suppresses insulin-like growth factor 1 activity in human KLE endometrial-like cells

In vivo (Athens, Greece) · 2004 · vol. 18(1) , pp. 43–7 · PMID:15011750 · W110628949
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Glucocorticoid receptor activation in human KLE cells suppressed IGF-1 and IGF-1.R mRNA expression and inhibited cell proliferation, an effect reversed by exogenous IGF-1.

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Abstract

We analysed the glucocorticoid receptor (GR) regulation on the expression of insulin-like growth factor 1 (IGF-1), type I IGF receptor (IGF-1.R), IGF-binding protein 3 (IGFBP-3), urokinase-type plasminogen activator (uPA) and uPA receptor (uPA.R) mRNA in human KLE endometrial-like cells. We documented that KLE cells express IGF-1, IGF-1.R, uPA and IGFBP-3 mRNA, however not uPA.R mRNA. Exogenous administration of dexamethasone inhibited the proliferation of KLE cells without inducing apoptosis. The inhibition of dexamethasone on KLE cell proliferation was neutralized by exogenous administration of IGF-1. Furthermore, dexamethasone suppressed the expression of IGF-1 mRNA and IGF-1.R mRNA as well as the IGF-1 bioavailability in KLE cell culture media, but it did not alter the expression of uPA mRNA and IGFBP-3 mRNA in KLE cells. Since the peritoneal fluid of women with endometriosis is known to contain IGF-1, which stimulates the proliferation and inhibits the apoptosis of endometrial-like cells, it is conceivable that GR-mediated down-regulation of IGF-1 bioavailability may be of clinical relevance for endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometrium Insulin-Like Growth Factor I Insulin-Like Growth Factor I Receptors, Glucocorticoid Cell Line Cell Line Dexamethasone Dexamethasone Dexamethasone Endometrium Endometrium Endometrium Endometrium Female Female Humans Humans Insulin-Like Growth Factor I Insulin-Like Growth Factor I Insulin-Like Growth Factor I

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Cited by (2)

SciLite annotations

organisms 2
human human
chemicals 3
dexamethasone dexamethasone dexamethasone

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