miR-151a-3p 调节 TNIK/PI3K/Akt 轴并影响多囊卵巢综合征的进展。

IF 1.7 4区 医学 Q3 OBSTETRICS & GYNECOLOGY
Ji Lin, Heng Lin, Weiwei Li, Jianfen Huang, Lanlan Chen, Ruotao Wang
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引用次数: 0

摘要

目的:多囊卵巢综合征(PCOS)是育龄妇女常见的生殖内分泌疾病:多囊卵巢综合征(PCOS)是育龄妇女常见的生殖内分泌疾病,近年来其发病率呈上升趋势。然而,该病的发病机制尚未完全阐明:方法:采用实时荧光定量聚合酶链反应(RT-qPCR)测定卵巢颗粒细胞(KGN)中 miR-151a-3p 的表达。使用细胞计数试剂盒-8(CCK-8)、集落形成和流式细胞仪检测 miR-151a-3p 对 KGN 细胞的影响。荧光素酶报告分析和 Western 印迹法用于验证 Traf 和 Nck 互作激酶(TNIK)对 miR-151a-3p 的靶向作用。免疫印迹(Western blotting,WB)用于评估蛋白水平:结果:我们发现,在多囊卵巢综合征患者的血清中,miR-151a-3p 下调,TNIK 上调。低表达的 miR-151a-3p 可促进细胞增殖、集落形成和 G0/G1 转换,减少细胞凋亡。我们的研究结果表明,低表达的 miR-151a-3p 促进了 TNIK 的表达,而 TNIK 激活了磷脂肌醇 3- 激酶/蛋白激酶 B(PI3K/Akt)通路。在卵巢颗粒细胞中,TNIK的过表达可挽救miR-151a-3p的作用。最后,我们的研究结果表明,在多囊卵巢综合征患者中,miR-151a-3p的表达与靶标TNIK的表达之间存在显著相关性,miR-151a-3p通过激活PI3K/AKT信号通路促进疾病的发生:结论:低表达的miR-151a-3p通过激活TNIK介导的PI3K/AKT信号通路促进KNG细胞增殖。miR-151a-3p/TNIK/PI3K/AKT信号轴可能是预防多囊卵巢综合征恶化的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
miR-151a-3p regulates the TNIK/PI3K/Akt axis and influences the progression of polycystic ovary syndrome.

Objectives: Polycystic ovarian syndrome (PCOS) is a common reproductive endocrine disease in women of childbearing age, and the incidence of PCOS has increased in recent years. However, the pathogenesis of this disease has not been fully elucidated.

Methods: The expression of miR-151a-3p in ovarian granulosa cells (KGN) was determined using real-time fluorescent quantitative polymerase chain reaction (RT-qPCR). Cell Counting Kit-8 (CCK-8), colony formation and flow cytometric assays were used to investigate the effect of miR-151a-3p on KGN cells. Luciferase reporter analysis and western blotting were used to verify the targeting of miR-151a-3p by Traf and Nck interacting kinase (TNIK). Western blotting (WB) was used to evaluate the protein levels.

Results: We found that miR-151a-3p was downregulated and TNIK was upregulated in the serum of PCOS patients. Low expression of miR-151a-3p promoted cell proliferation, colony formation and the G0/G1 transition and reduced apoptosis. Our results showed that low expression of miR-151a-3p promoted the expression of TNIK, which activated the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway. Overexpression of TNIK rescued the effect of miR-151a-3p in ovarian granulosa cells. Finally, our results showed that there was a significant correlation between the expression of miR-151a-3p and the expression of the target TNIK in PCOS patients and that miR-151a-3p promoted disease occurrence by activating the PI3K/AKT signaling pathway.

Conclusions: Low expression of miR-151a-3p promoted KNG cell proliferation by activating the TNIK-mediated PI3K/AKT signaling pathway. The miR-151a-3p/TNIK/PI3K/AKT signaling axis may be a potential therapeutic target for preventing the progression of PCOS.

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来源期刊
CiteScore
4.40
自引率
0.00%
发文量
217
审稿时长
2-3 weeks
期刊介绍: The official journal of The European Association of Perinatal Medicine, The Federation of Asia and Oceania Perinatal Societies and The International Society of Perinatal Obstetricians. The journal publishes a wide range of peer-reviewed research on the obstetric, medical, genetic, mental health and surgical complications of pregnancy and their effects on the mother, fetus and neonate. Research on audit, evaluation and clinical care in maternal-fetal and perinatal medicine is also featured.
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