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J. Biol. Chem., Vol. 277, Issue 29, 26208-26216, July 19, 2002
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From the We investigated the regulation of prostaglandin
production in normal endometrial stromal cells (ESC) by malignant
endometrial epithelial cells. We found that cyclooxygenase (COX)-2
mRNA and protein levels and prostaglandin (PG)E2
production in ESC were significantly increased by Ishikawa malignant
endometrial epithelial cell conditioned medium (MECM). By using
transient transfection assays, we found that the
Up-regulation of Cyclooxygenase-2 Expression and Prostaglandin
Synthesis in Endometrial Stromal Cells by Malignant Endometrial
Epithelial Cells
A PARACRINE EFFECT MEDIATED BY PROSTAGLANDIN E2 AND
NUCLEAR FACTOR-
B*
,,,,
, and**
Departments of Obstetrics and Gynecology and
Molecular Genetics and the § Department of Pathology, the
University of Illinois, Chicago, Illinois 60612 and the
¶ Department of Pathology and the Department of Obstetrics
and Gynecology, Tohoku University School of Medicine,
Sendai 980-8574, Japan
360/218-bp region
of the COX-2 promoter gene was critical for MECM
induction of promoter activity. This MECM-responsive region contained a
variant nuclear factor (NF)-B site at 222 to 213 that, when
mutated, completely abolished COX-2 promoter activation by
MECM. Employing electrophoretic mobility shift assays, we further
demonstrated that binding of NF-B p65 to this NF-B-binding site
is, in part, responsible for the COX-2 promoter activation
by MECM. To investigate further the potential effects of MECM on
COX-2 mRNA stability, ESC were treated with MECM in the
absence or presence of actinomycin D, a general transcription inhibitor. We found that MECM significantly increased COX-2
mRNA stability. Intriguingly, we found that PGE2 was
one of the major factors in MECM, which was responsible for
up-regulating COX-2 expression in ESC. ECC-1 and HEC-1A malignant
endometrial epithelial cell lines also produced significantly increased
quantities of PGE2. In conclusion, malignant endometrial
epithelial cells secrete PGE2 that induces COX-2 expression
in normal endometrial stromal cells in a paracrine fashion through
activation of transcription and stabilization of COX-2 mRNA.
*
This work was supported by National Institutes of Health
Grant HD38691 (to S. E. B.) and by a fellowship award (to M. T.) from the Japan Menopause Society, Tokyo, Japan.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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