Department of Gynaecology, Shanghai Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
Mol Med Rep. 2021 May;23(5). doi: 10.3892/mmr.2021.11995. Epub 2021 Mar 24.
Endometriosis (EM) is a multifactorial and debilitating chronic benign gynecological disease, but the pathogenesis of the disease is not completely understood. Dysregulated expression of microRNAs (miRNA/miR) is associated with the etiology of EM due to their role in regulating endometrial stromal cell proliferation and invasion. The present study aimed to identify the functions and mechanisms underlying miR‑143‑3p in EM. To explore the role of miR‑143‑3p in EM, functional miRNAs were analyzed via bioinformatics analysis. miR‑143‑3p expression levels in endometriotic stromal cells (ESCs) and normal endometrial stromal cells (NESCs) were measured via reverse transcription‑quantitative PCR. The role of miR‑143‑3p in regulating ESC proliferation and invasion was assessed by performing Cell Counting Kit‑8 and Transwell assays, respectively. miR‑143‑3p expression was significantly upregulated in ESCs compared with NESCs. Functionally, miR‑143‑3p overexpression inhibited ESC proliferation and invasion, whereas miR‑143‑3p knockdown promoted ESC proliferation and invasion. Moreover, miR‑143‑3p inhibited autophagy activation in ESCs, as indicated by decreased green puncta, which represented autophagic vacuoles, decreased microtubule associated protein 1 light chain 3α expression and increased p62 expression in the miR‑143‑4p mimic group compared with the control group. Moreover, compared with the control group, miR‑143‑3p overexpression significantly decreased the expression levels of autophagy‑related 2B (ATG2B), a newly identified target gene of miR‑143‑3p, in ESCs. ATG2B overexpression reversed miR‑143‑3p overexpression‑mediated inhibition of ESC proliferation and invasion. Collectively, the results of the present study suggested that miR‑143‑3p inhibited EM progression, thus providing a novel target for the development of therapeutic agents against EM.
子宫内膜异位症（EM）是一种多因素、使人虚弱的慢性良性妇科疾病，但疾病的发病机制尚不完全清楚。由于 microRNAs（miRNA/miR）在调节子宫内膜基质细胞增殖和侵袭中的作用，其表达失调与 EM 的病因有关。本研究旨在确定 miR-143-3p 在 EM 中的功能和机制。为了探讨 miR-143-3p 在 EM 中的作用，通过生物信息学分析分析了功能 miRNA。通过逆转录-定量 PCR 测量了子宫内膜异位症基质细胞（ESCs）和正常子宫内膜基质细胞（NESCs）中 miR-143-3p 的表达水平。通过 Cell Counting Kit-8 和 Transwell 测定分别评估 miR-143-3p 调节 ESC 增殖和侵袭的作用。与 NESCs 相比，ESCs 中 miR-143-3p 的表达明显上调。功能上，miR-143-3p 过表达抑制 ESC 增殖和侵袭，而 miR-143-3p 敲低促进 ESC 增殖和侵袭。此外，miR-143-3p 抑制 ESCs 中的自噬激活，表现为绿色斑点减少，代表自噬空泡，miR-143-4p 模拟物组与对照组相比，微管相关蛋白 1 轻链 3α 表达减少和 p62 表达增加。此外，与对照组相比，miR-143-3p 过表达显着降低了 ESCs 中自噬相关 2B（ATG2B）的表达水平，ATG2B 是 miR-143-3p 的新鉴定靶基因。ATG2B 过表达逆转了 miR-143-3p 过表达介导的 ESC 增殖和侵袭抑制。综上所述，本研究结果表明，miR-143-3p 抑制 EM 进展，从而为开发针对 EM 的治疗药物提供了新的靶点。
