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Updated: Jul 11, 2026
Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
Published on: March 17, 2016
Estrogen up-regulates cyclooxygenase-2 via estrogen receptor in human uterine microvascular endothelial cells
Mitsutoshi Tamura1, Santanu Deb, Siby Sebastian
1Departments of Obstetrics and Gynecology and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois 60611, USA.
Objective:
To investigate the effects of 17beta-estradiol (E(2)) on cyclooxygenase-2 (COX-2) expression and prostaglandin E(2) (PGE(2)) synthesis in primary human uterine microvascular endothelial cells (HUMEC).
Design:
Prospective study.
Setting:
Basic research laboratory at an academic medical center.
Patient(S):
Primary HUMEC of three women donors and primary human dermal microvascular endothelial cells of three women donors (as control), purchased from a third-party source.
Intervention(S):
The HUMEC were cultured in specific media in a humidified atmosphere with 5% CO(2) at 37 degrees C.
Main Outcome Measure(S):
Measures of COX-2 mRNA and protein, PGE(2) production, and estrogen receptor alpha and beta mRNA and protein.
Result(S):
Treatment with E(2) (10(-10) to 10(-6) M) increased COX-2 mRNA levels by 2.3-fold to 2.4-fold in HUMEC. Treatment of HUMEC with E(2) (10(-8) M) resulted in a time-dependent increase of COX-2 mRNA levels. This was accompanied by a 2.8-fold increase in COX-2 protein level and a 1.5-fold increase in PGE(2) synthesis. Pretreatment of HUMEC with a selective COX-2 inhibitor, NS-398, abolished E(2)-induced PGE(2) synthesis, suggesting that E(2) specifically up-regulates COX-2 activity. The estrogen receptor antagonist ICI 182,780 fully reversed the stimulation of COX-2 mRNA and protein levels and PGE(2) synthesis by E(2). Interestingly, estrogen receptor beta mRNA and protein were abundant in HUMEC, whereas estrogen receptor alpha mRNA or protein was barely detectable.
Conclusion(S):
We conclude that various levels of E(2) can significantly increase COX-2 expression and PGE(2) synthesis in HUMEC via the estrogen receptor.
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