miR-34a-5p modulation of polycystic ovary syndrome via targeting the NOTCH signaling pathway

多囊卵巢 Notch信号通路 医学 卵巢 生殖医学 信号转导 内分泌学 细胞生物学 内科学 生物 受体 怀孕 遗传学 糖尿病 胰岛素抵抗
作者
Kexin Zhang,Xiaomeng Wang,Fang Liu,Hong Lin,Yan Wang,Min Zhao,Xiaofei Wang,Yijing Chu,Lin Xu
出处
期刊:Journal of Ovarian Research [Springer Nature]
卷期号:18 (1): 55-55 被引量:3
标识
DOI:10.1186/s13048-025-01623-4
摘要

Polycystic ovary syndrome (PCOS) is currently recognized as a condition that affects several systems in the body, including the reproductive, endocrine, and cardiovascular systems. Prevalent among teenagers and women of reproductive age. Prior research has demonstrated an elevation of miR-34a-5p within the follicular fluid (FF) of women of PCOS. Despite this, the precise mechanisms through which miR-34a-5p influences granulosa cells (GC) development and function remain poorly characterized. Therefore, this study investigates the involvement and pathogenic mechanisms of miR-34a-5p within GCs in the context of PCOS. The human granulosa-like tumor cell line (KGN) got transfected at a control, as well as a miR-34a-5p mimic and inhibitor, respectively. Monitor cellular proliferation in each experimental group. The experimental methods included RT-qPCR, CCK8, flow cytometry and western blotting. Also, the interaction between miR-34a-5p and the particular sequence of JAG1 has been verified using the dual luciferase assay. Further investigation of the connection involving miR-34a-5p and the Notch signaling pathway was conducted using bioinformatics analysis and experimental methods. The results demonstrated that miR-34a-5p expression was significantly elevated in the serum(p<0. 0001)and FF (p = 0. 0402) of PCOS, whereas its expression in GCs (p = 0. 5522) showed no significant variation. Overexpressing miR-34a-5p caused a decrease in the rate at which KGN cells multiplied and an increase in programmed cell death. Conversely, inhibiting miR-34a-5p resulted in an increase in cell growth and a decrease in programmed cell death. Bioinformatics analysis and experimental results further demonstrated thatmiR-34a-5p interacts with the 3'UTR region of JAG1, leading to a negative regulation of the Jagged1-Notch signaling pathway. In summary, the miR-34a-5p molecule inhibits the growth of GCs as well as triggers programmed cell death by regulating the Jagged1-Notch signaling pathway. Silencing miR-34a-5p prevents dysfunction in GCs. Our analysis implies that miR-34a-5p is a new molecular site to treat PCOS.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
任性依玉完成签到,获得积分20
刚刚
LCC完成签到 ,获得积分10
1秒前
1秒前
小陈想毕业完成签到,获得积分10
1秒前
无情的谷兰完成签到,获得积分10
1秒前
1秒前
11完成签到,获得积分10
2秒前
自由盼夏完成签到 ,获得积分10
2秒前
贝卓飞完成签到,获得积分10
3秒前
zhou123432发布了新的文献求助10
3秒前
研友_LmVygn发布了新的文献求助10
3秒前
任性依玉发布了新的文献求助10
3秒前
舒心新儿应助楠木采纳,获得10
3秒前
mirrovo完成签到 ,获得积分10
3秒前
wx发布了新的文献求助30
4秒前
丘比特应助小花采纳,获得10
4秒前
4秒前
MM完成签到,获得积分10
5秒前
康明雪完成签到,获得积分10
5秒前
5秒前
ztt1221完成签到,获得积分10
6秒前
ding应助ppf采纳,获得10
6秒前
6秒前
6秒前
丽颖发布了新的文献求助10
7秒前
陶嘉云完成签到,获得积分10
7秒前
安静的猴子完成签到 ,获得积分10
7秒前
7秒前
zjjcug完成签到,获得积分10
8秒前
胡萝卜完成签到 ,获得积分10
8秒前
完美世界应助活力的紫菜采纳,获得10
8秒前
田様应助14122采纳,获得10
9秒前
Ice完成签到,获得积分10
9秒前
轻松博超完成签到,获得积分10
9秒前
三叶草完成签到,获得积分10
9秒前
人间烟火完成签到,获得积分10
10秒前
2哇哇哇发布了新的文献求助10
10秒前
camellia完成签到,获得积分10
10秒前
赘婿应助brd采纳,获得10
10秒前
文静的怜烟完成签到,获得积分10
11秒前
高分求助中
Encyclopedia of Quaternary Science Third edition 2025 12000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
The Social Work Ethics Casebook: Cases and Commentary (revised 2nd ed.). Frederic G. Reamer 800
Beyond the sentence : discourse and sentential form / edited by Jessica R. Wirth 600
Holistic Discourse Analysis 600
Vertébrés continentaux du Crétacé supérieur de Provence (Sud-Est de la France) 600
Vertebrate Palaeontology, 5th Edition 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 纳米技术 计算机科学 内科学 化学工程 复合材料 物理化学 基因 遗传学 催化作用 冶金 量子力学 光电子学
热门帖子
关注 科研通微信公众号,转发送积分 5337659
求助须知:如何正确求助?哪些是违规求助? 4474834
关于积分的说明 13926106
捐赠科研通 4369836
什么是DOI,文献DOI怎么找? 2401032
邀请新用户注册赠送积分活动 1394060
关于科研通互助平台的介绍 1365964