Decorin induced by progesterone plays a crucial role in suppressing endometriosis

Yoshihiro Joshua Ono, Yoshito Terai, Akiko Tanabe, Atsushi Hayashi, Masami Hayashi, Yoshiki Yamashita, Satoru Kyo, Masahide Ohmichi
The Journal of endocrinology · 2014 · vol. 223(2) , pp. 203–216 · doi:10.1530/joe-14-0393 · PMID:25244916 · W2097253499
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Progesterone and dienogest inhibit ectopic endometrial cell growth and induce cell cycle arrest by increasing decorin and p21 expression, while also suppressing MET.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 ⓘ

This study examined how progesterone and the progestin dienogest affect proliferation and cell-cycle regulation in human endometriotic cell lines, focusing on the role of the progesterone-inducible proteoglycan decorin (DCN). In vitro, both decorin and dienogest inhibited dose-dependent growth of ectopic endometrial epithelial and stromal cell lines, with chromatin immunoprecipitation showing that progesterone/dienogest induced binding to the decorin promoter, and that decorin-associated p21 induction mediated cell-cycle arrest; decorin also suppressed MET expression. In a retrospective cross-sectional study of 50 endometriosis patients, DCN mRNA was higher in ovarian endometrioma samples from patients treated with dienogest than in controls, but the paper’s clinical component does not prove causality and relies on a limited observational design. This paper is centrally about endometriosis — it shows progesterone/dienogest suppresses endometriotic cell growth via decorin and p21-mediated cell cycle arrest.

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Abstract

Dienogest, a synthetic progestin, has been shown to be effective against endometriosis, although it is still unclear as to how it affects the ectopic endometrial cells. Decorin has been shown to be a powerful endogenous tumor repressor acting in a paracrine fashion to limit tumor growth. Our objectives were to examine the direct effects of progesterone and dienogest on the in vitro proliferation of the human ectopic endometrial epithelial and stromal cell lines, and evaluate as to how decorin contributes to this effect. We also examined DCN mRNA expression in 50 endometriosis patients. The growth of both cell lines was inhibited in a dose-dependent manner by both decorin and dienogest. Using a chromatin immunoprecipitation assay, it was noted that progesterone and dienogest directly induced the binding of the decorin promoter in the EMOsis cc/TERT cells (immortalized human ovarian epithelial cells) and CRL-4003 cells (immortalized human endometrial stromal cells). Progesterone and dienogest also led to significant induced cell cycle arrest via decorin by promoting production of p21 in both cell lines in a dose-dependent manner. Decorin also suppressed the expression of MET in both cell lines. We confirmed that DCN mRNA expression in patients treated with dienogest was higher than that in the control group. In conclusion, decorin induced by dienogest appears to play a crucial role in suppressing endometriosis by exerting anti-proliferative effects and inducing cell cycle arrest via the production of p21 human ectopic endometrial cells and eutopic endometrial stromal cells.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Decorin Endometriosis Endometriosis Ovarian Diseases Ovarian Diseases Progesterone Adult Cell Cycle Cell Cycle Cell Cycle Cells, Cultured Cross-Sectional Studies Decorin Decorin Endometriosis Endometriosis Female Humans Middle Aged Nandrolone

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