Regulatory mechanism of GPER in the invasion and migration of ectopic endometrial stromal cells in endometriosis.

IF 1.2 4区医学 Q4 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH Women & Health Pub Date : 2024-02-07 Epub Date: 2024-01-30 DOI:10.1080/03630242.2023.2296522

Hongyan Shi, Kejun Xu, Mengna Huang, Meiya Mao, Jilan Ou

{"title":"Regulatory mechanism of GPER in the invasion and migration of ectopic endometrial stromal cells in endometriosis.","authors":"Hongyan Shi, Kejun Xu, Mengna Huang, Meiya Mao, Jilan Ou","doi":"10.1080/03630242.2023.2296522","DOIUrl":null,"url":null,"abstract":"<p><p>Endometriosis (EMS) is a chronic inflammatory disorder of high incidence that causes serious reproductive consequences. High estrogen production is a consistently observed endocrine feature of EMS. The present study aims to probe the molecular mechanism of G protein-coupled estrogen receptor 1 (GPER) in the invasion and migration of ectopic endometrial stromal cells (Ect-ESCs) and provides a new rationale for EMS treatment. Eutopic and ectopic endometrial tissues were collected from 41 EMS patients, and primary ESCs were separated. GPER, miR-16-5p, and miR-103a-3p levels in cells and tissues were determined by qRT-PCR or Western blot assay. Cell viability, proliferation, invasion, and migration were evaluated by CCK-8, colony formation, and Transwell assays. The upstream miRNAs of GPER were predicted by databases, and dual-luciferase assay was performed to validate the binding of miR-16-5p and miR-103a-3p to GPER 3'UTR. GPER was highly expressed in EMS tissues and Ect-ESCs. Inhibition of GPER mitigated the proliferation, invasion, and migration of Ect-ESCs. GPER was regulated by miR-16-5p and miR-103a-3p. Overexpression of miR-16-5p and miR-103a-3p negatively regulated GPER expression and inhibited the invasion and migration of Ect-ESC. In conclusion, GPER promoted the invasion and migration of Ect-ESCs, which can be reversed by upstream miR-16-5p and miR-103a-3p.</p>","PeriodicalId":23972,"journal":{"name":"Women & Health","volume":null,"pages":null},"PeriodicalIF":1.2000,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Women & Health","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/03630242.2023.2296522","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/30 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH","Score":null,"Total":0}

引用次数: 0

Abstract

Endometriosis (EMS) is a chronic inflammatory disorder of high incidence that causes serious reproductive consequences. High estrogen production is a consistently observed endocrine feature of EMS. The present study aims to probe the molecular mechanism of G protein-coupled estrogen receptor 1 (GPER) in the invasion and migration of ectopic endometrial stromal cells (Ect-ESCs) and provides a new rationale for EMS treatment. Eutopic and ectopic endometrial tissues were collected from 41 EMS patients, and primary ESCs were separated. GPER, miR-16-5p, and miR-103a-3p levels in cells and tissues were determined by qRT-PCR or Western blot assay. Cell viability, proliferation, invasion, and migration were evaluated by CCK-8, colony formation, and Transwell assays. The upstream miRNAs of GPER were predicted by databases, and dual-luciferase assay was performed to validate the binding of miR-16-5p and miR-103a-3p to GPER 3'UTR. GPER was highly expressed in EMS tissues and Ect-ESCs. Inhibition of GPER mitigated the proliferation, invasion, and migration of Ect-ESCs. GPER was regulated by miR-16-5p and miR-103a-3p. Overexpression of miR-16-5p and miR-103a-3p negatively regulated GPER expression and inhibited the invasion and migration of Ect-ESC. In conclusion, GPER promoted the invasion and migration of Ect-ESCs, which can be reversed by upstream miR-16-5p and miR-103a-3p.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

GPER 在子宫内膜异位症异位子宫内膜基质细胞侵袭和迁移中的调控机制。

子宫内膜异位症（EMS）是一种发病率很高的慢性炎症性疾病，会对生殖系统造成严重影响。雌激素分泌旺盛是 EMS 一直以来的内分泌特征。本研究旨在探究G蛋白偶联雌激素受体1（GPER）在异位子宫内膜基质细胞（Ect-ESCs）侵袭和迁移过程中的分子机制，为EMS的治疗提供新的理论依据。研究人员收集了41名EMS患者的异位和异位子宫内膜组织，并分离了原代ESCs。通过 qRT-PCR 或 Western 印迹法测定细胞和组织中 GPER、miR-16-5p 和 miR-103a-3p 的水平。细胞活力、增殖、侵袭和迁移通过 CCK-8、菌落形成和 Transwell 试验进行评估。通过数据库预测了GPER的上游miRNA，并用双荧光素酶试验验证了miR-16-5p和miR-103a-3p与GPER 3'UTR的结合。GPER在EMS组织和Ect-ESC中高表达。抑制GPER可减轻Ect-ESCs的增殖、侵袭和迁移。GPER受miR-16-5p和miR-103a-3p调控。过表达 miR-16-5p 和 miR-103a-3p 会负向调节 GPER 的表达，并抑制 Ect-ESC 的侵袭和迁移。总之，GPER能促进Ect-ESC的侵袭和迁移，而上游的miR-16-5p和miR-103a-3p能逆转GPER的表达。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Women & Health Multiple-

CiteScore

2.70

自引率

0.00%

发文量

期刊介绍： Women & Health publishes original papers and critical reviews containing highly useful information for researchers, policy planners, and all providers of health care for women. These papers cover findings from studies concerning health and illness and physical and psychological well-being of women, as well as the environmental, lifestyle and sociocultural factors that are associated with health and disease, which have implications for prevention, early detection and treatment, limitation of disability and rehabilitation.