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异常上调的 miR-142-3p 通过调节 FOXM1 抑制滋养层细胞的增殖和侵袭。

Aberrantly up-regulated miR-142-3p inhibited the proliferation and invasion of trophoblast cells by regulating FOXM1.

机构信息

Department of Obstetrics, Gansu Provincial Hospital, Lanzhou, Gansu, 730000, China.

Department of Radiology, Gansu Gem Flower Hospital, Lanzhou, Gansu, 730060, China.

出版信息

Placenta. 2021 Jan 15;104:253-260. doi: 10.1016/j.placenta.2021.01.002. Epub 2021 Jan 6.

Abstract

INTRODUCTION

Preeclampsia is one of the main causes of morbidity and mortality in pregnant women and mothers. Numerous studies showed that microRNAs (miRNAs) played important roles in the occurrence and development of preeclampsia. However, the regulation of microRNA-142-3p (miR-142-3p) in preeclampsia has not been clarified.

METHODS

The expression of miR-142-3p and FOXM1 was detected by RT-qPCR. The interaction between miR-142-3p and FOXM1 was confirmed by dual-luciferase reporter assay. The relative protein expression of FOXM1 was measured by western blot. Cell proliferation was measured using MTT assay. Cell migration was detected using transwell assay and wound healing assay.

RESULTS

The expression of miR-142-3p was up-regulated, while the mRNA and protein of FOXM1 expression were down-regulated in preeclampsia tissues. Additionally, we found that miR-142-3p targeted FOXM1. Moreover, FOXM1 expression was negatively regulated by miR-142-3p. Functional experiments showed that overexpression of miR-142-3p inhibited cell growth and migration in trophoblast cells. Reverse experiments determined that overexpression of FOXM1 reversed the suppressive effects of miR-142-3p on cell proliferation and migration.

DISCUSSION

Our results demonstrated that miR-142-3p regulated cell proliferation and migration through targeting FOXM1 in trophoblast cells, providing a novel therapeutic target and extending the pathogenesis of preeclampsia.

摘要

简介

子痫前期是孕妇和产妇发病率和死亡率的主要原因之一。许多研究表明 microRNAs(miRNAs)在子痫前期的发生和发展中起重要作用。然而,miR-142-3p 在子痫前期中的调节作用尚不清楚。

方法

通过 RT-qPCR 检测 miR-142-3p 和 FOXM1 的表达。通过双荧光素酶报告基因实验证实 miR-142-3p 和 FOXM1 之间的相互作用。通过 Western blot 测定 FOXM1 的相对蛋白表达。使用 MTT 法测量细胞增殖。通过 Transwell 测定和划痕愈合测定检测细胞迁移。

结果

子痫前期组织中 miR-142-3p 的表达上调,而 FOXM1 的 mRNA 和蛋白表达下调。此外,我们发现 miR-142-3p 靶向 FOXM1。此外,miR-142-3p 负调控 FOXM1 的表达。功能实验表明,miR-142-3p 的过表达抑制滋养细胞的生长和迁移。反转实验确定,FOXM1 的过表达逆转了 miR-142-3p 对细胞增殖和迁移的抑制作用。

讨论

我们的结果表明,miR-142-3p 通过靶向滋养细胞中的 FOXM1 调节细胞增殖和迁移,为子痫前期的治疗提供了新的靶点,并扩展了子痫前期的发病机制。

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