Dienogest, a synthetic progestin, inhibits prostaglandin E2 production and aromatase expression by human endometrial epithelial cells in a spheroid culture system

Yutaka Shimizu, Shimizu Y, Mita S, Shizuka Mita, Takashi Takeuchi, Takeuchi T, Notsu T, Tatsuto Notsu, Kiyoshi Mizuguchi, Mizuguchi K, Satoru Kyo, Kyo S
Steroids · 2010 · vol. 76(1-2) , pp. 60–67 · doi:10.1016/j.steroids.2010.08.010 · PMID:20851710 · W1974214512
article OA: closed CC0 ⤵ 54 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Dienogest, a synthetic progestin, was found to suppress prostaglandin E2 production and aromatase expression in human endometrial epithelial cells cultured as spheroids.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Prostaglandin E(2) (PGE(2)) is a major mediator in the pathophysiology, and pathogenesis of gynecological diseases associated with abnormal endometrial disease with proliferation and inflammation, such as endometriosis. In this study, we investigated the effect of dienogest, a selective progesterone receptor agonist, on PGE(2) production and the expression of aromatase, an estrogen synthase, in human immortalized endometrial epithelial cells. Compared with monolayer culture, the cells showed enhanced PGE(2) production and expression of the PGE(2) synthases cyclooxygenase-2 (COX-2), and microsomal prostaglandin E(2) synthase-1 (mPGES-1) in a spheroid culture system. Dienogest inhibited PGE(2) production and this effect was reversed by RU486, a progesterone receptor antagonist. Dienogest inhibited the PGE(2) synthases mRNA and protein expression, and the nuclear factor-κB activation. Moreover, the suppressive effect of dienogest on PGE(2) production was sustained 24h after the drug was withdrawn. Dienogest but not COX inhibitors inhibited aromatase expression. These results suggest that progesterone receptor activation reduces the gene expressions of COX-2, mPGES-1, and aromatase. Our findings suggest that the pharmacological mechanism of dienogest includes the direct inhibition of PGE(2) synthase and aromatase expression and may contribute to the therapeutic effect on the progression of endometriosis.

My notes (saved in your browser only)

MeSH descriptors

Aromatase Dinoprostone Endometrium Epithelial Cells Nandrolone Spheroids, Cellular Aromatase Aromatase Cell Culture Techniques Cells, Cultured Dinoprostone Dinoprostone Endometrium Endometrium Endometrium Epithelial Cells Epithelial Cells Epithelial Cells Female Humans

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (36)

Cited by (50)

Source provenance

europepmc
last seen: 2026-08-06T06:07:45.168820+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:17:00.782903+00:00
License: CC0 · commercial use OK