Cell proliferation mechanism via estrogen-related receptors in endometriosis

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10681
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: Kitawaki Jo 京都府立医科大学, 医学(系)研究科(研究院), 教授 (00204925)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 子宮内膜症 / エストロゲン関連受容体 / GPER1 / アグリコン型イソフラボン

Outline of Final Research Achievements

Endometriosis is one of estrogen-dependent diseases. In endometriosis tissue, the expression level of estrogen receptor (ER)β is higher than that of ERα. Endometriosis also expresses estrogen-related receptor (ERR) α, β, γ, and a transmembrane receptor GPER1.
Using primary cultured cell line derived from endometriosis and mouse endometriosis model, we demonstrated that G1, a GPER1 agonist, induces apoptosis by non-genomic action. Furthermore, we demonstrated that AglyMAX, an aglycone-type isoflavone with weak estrogen action, suppresses proliferation of endometriotic cells and cystic lesion of mouse model via the ERβ-NFκB pathway. AglyMAX inhibits various inflammatory factors.

Free Research Field

産婦人科学