MiR-19b-3p inhibits cell viability and proliferation and promotes apoptosis by targeting IGF1 in KGN cells.

IF 2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Gynecological Endocrinology Pub Date : 2024-12-01 Epub Date: 2024-11-06 DOI:10.1080/09513590.2024.2425318
Youzhu Li, Yuanyuan Ye, Hengyuan Zhang, Ye Yang, Ningqing Zhang, Hong Gao, Rongfeng Wu
{"title":"MiR-19b-3p inhibits cell viability and proliferation and promotes apoptosis by targeting IGF1 in KGN cells.","authors":"Youzhu Li, Yuanyuan Ye, Hengyuan Zhang, Ye Yang, Ningqing Zhang, Hong Gao, Rongfeng Wu","doi":"10.1080/09513590.2024.2425318","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Endometriosis (EM) is a major cause of infertility, but the pathogenesis and mechanisms are not yet fully elucidated. MiR-19b-3p is involved in many diseases, but its functional role in EM-associated infertility remains unexplored. This study aimed to examine miR-19b-3p abundance and IGF1 concentration in cumulus cells (CCs) and follicular fluid of EM-associated infertility patients, and to investigate the potential role of miR-19b-3p in KGN cells by identifying its target and elucidating the underlying mechanisms.</p><p><strong>Results: </strong>The results from the case-control study indicated that, compared to the control group consisting of patients with tubal infertility, patients with EM-associated infertility exhibited a lower percentage of mature oocytes. MiR-19b-3p level was elevated in CCs from EM-associated infertility patients. IGF1 was identified as a direct target of miR-19b-3p and was negatively regulated by miR-19b-3p in KGN cells. Overexpression of miR-19b-3p significantly inhibited cell viability and proliferation, promoted apoptosis, and arrested the cell cycle at G0/G1 phase in KGN cells. The effects of miR-19b-3p were reversed by co-transfection of IGF1, and the biological effects of miR-19b-3p in KGN cells were mediated by IGF1. Additionally, miR-19b-3p targeted IGF1 to down-regulate AKT phosphorylation and participate in the apoptotic pathway in KGN cells.</p><p><strong>Conclusions: </strong>This study demonstrates that miR-19b-3p level is elevated in CCs and IGF1 concentration is decreased in follicular fluid in patients with EM-associated infertility. MiR-19b-3p regulates the biological effects of KGN cells by targeting IGF1.</p>","PeriodicalId":12865,"journal":{"name":"Gynecological Endocrinology","volume":"40 1","pages":"2425318"},"PeriodicalIF":2.0000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gynecological Endocrinology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/09513590.2024.2425318","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/11/6 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Endometriosis (EM) is a major cause of infertility, but the pathogenesis and mechanisms are not yet fully elucidated. MiR-19b-3p is involved in many diseases, but its functional role in EM-associated infertility remains unexplored. This study aimed to examine miR-19b-3p abundance and IGF1 concentration in cumulus cells (CCs) and follicular fluid of EM-associated infertility patients, and to investigate the potential role of miR-19b-3p in KGN cells by identifying its target and elucidating the underlying mechanisms.

Results: The results from the case-control study indicated that, compared to the control group consisting of patients with tubal infertility, patients with EM-associated infertility exhibited a lower percentage of mature oocytes. MiR-19b-3p level was elevated in CCs from EM-associated infertility patients. IGF1 was identified as a direct target of miR-19b-3p and was negatively regulated by miR-19b-3p in KGN cells. Overexpression of miR-19b-3p significantly inhibited cell viability and proliferation, promoted apoptosis, and arrested the cell cycle at G0/G1 phase in KGN cells. The effects of miR-19b-3p were reversed by co-transfection of IGF1, and the biological effects of miR-19b-3p in KGN cells were mediated by IGF1. Additionally, miR-19b-3p targeted IGF1 to down-regulate AKT phosphorylation and participate in the apoptotic pathway in KGN cells.

Conclusions: This study demonstrates that miR-19b-3p level is elevated in CCs and IGF1 concentration is decreased in follicular fluid in patients with EM-associated infertility. MiR-19b-3p regulates the biological effects of KGN cells by targeting IGF1.

MiR-19b-3p 通过靶向 IGF1 抑制 KGN 细胞的活力和增殖,并促进细胞凋亡。
背景:子宫内膜异位症(EM)是导致不孕的主要原因之一,但其发病机制尚未完全阐明。MiR-19b-3p参与了许多疾病的治疗,但它在EM相关不孕症中的功能作用仍未得到探讨。本研究旨在检测EM相关性不孕症患者精原细胞(CCs)和卵泡液中miR-19b-3p的丰度和IGF1的浓度,并通过确定miR-19b-3p的靶点和阐明其潜在机制,研究miR-19b-3p在KGN细胞中的潜在作用:病例对照研究结果表明,与输卵管性不孕患者组成的对照组相比,EM相关性不孕患者的成熟卵母细胞比例较低。在EM相关性不孕症患者的CC中,MiR-19b-3p水平升高。研究发现,IGF1是miR-19b-3p的直接靶标,并在KGN细胞中受miR-19b-3p的负调控。过表达 miR-19b-3p 能明显抑制 KGN 细胞的活力和增殖,促进细胞凋亡,并使细胞周期停滞在 G0/G1 期。同时转染 IGF1 后,miR-19b-3p 的作用被逆转,miR-19b-3p 对 KGN 细胞的生物效应是由 IGF1 介导的。此外,miR-19b-3p靶向IGF1下调AKT磷酸化,参与KGN细胞的凋亡通路:本研究表明,在EM相关性不孕症患者中,CCs中的miR-19b-3p水平升高,卵泡液中的IGF1浓度降低。MiR-19b-3p通过靶向IGF1调节KGN细胞的生物学效应。
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 求助全文
来源期刊
Gynecological Endocrinology
Gynecological Endocrinology 医学-妇产科学
CiteScore
4.40
自引率
5.00%
发文量
137
审稿时长
3-6 weeks
期刊介绍: Gynecological Endocrinology , the official journal of the International Society of Gynecological Endocrinology, covers all the experimental, clinical and therapeutic aspects of this ever more important discipline. It includes, amongst others, papers relating to the control and function of the different endocrine glands in females, the effects of reproductive events on the endocrine system, and the consequences of endocrine disorders on reproduction
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信