Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p

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This study found that NEAT1 expression is increased in endometriosis, and silencing it inhibits cell proliferation, migration, and invasion while promoting apoptosis by targeting miR-124-3p.

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The paper investigates the lncRNA NEAT1 and its proposed mechanism in endometriosis (EM), using endometrial tissues from an EM rat model and from patients, and isolating endometrial stromal cells from ectopic (EC) versus eutopic (EU) endometrium. NEAT1 and miR-124-3p were measured by RT-qPCR, and EC-ESC functional effects of NEAT1 or miR-124-3p modulation were tested using MTT, flow cytometry, western blotting, and Transwell assays, with NEAT1–miR-124-3p targeting validated by dual-luciferase and co-transfection experiments. NEAT1 was upregulated and miR-124-3p downregulated in EM tissues and EC-ESCs, and silencing NEAT1 inhibited proliferation, migration, and invasion while promoting apoptosis via miR-124-3p. The study does not specify key limitations in the abstract beyond a focus on cellular and expression changes; This paper is centrally about endometriosis — it examines NEAT1 upregulation in ectopic endometrial stromal cells and its regulation of EC-ESC behaviors through miR-124-3p.

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Abstract

BackgroundEndometriosis (EM) is a gynecological disease that poses severe health risks to women, although its pathogenesis has yet to be fully elucidated. It has been shown that long non-coding RNAs (lncRNAs) are closely associated with EM initiation and have a role in the development of this disease. Previous studies exploring the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) have shown that this lncRNA functions as a tumor promoter in endometrial cancer. However, its exact mechanism of action in EM remains unclear.ObjectiveThis report was designed to illustrate the potential molecular mechanisms of lncRNA NEAT1 on EM.MethodsEndometrial tissues were extracted from EM model rats and patients with EM. Hematoxylin and eosin staining was applied to detect the morphological changes that occurred in rats after construction of the model. Endometrial stromal cells (ESCs) were extracted from either ectopic endometrium (EC) or eutopic endometrium (EU) tissues from patients with EM. LncRNA NEAT1 and miR-124-3p expression in EM tissues and cells were subsequently evaluated by reverse transcription-quantitative (RT-q)PCR analysis. MTT assay, flow cytometric analysis, western blot assay and Transwell assay were then employed to examine the effect of NEAT1 and miR-124-3p on EC-ESC proliferation, apoptosis, migration and invasion, respectively. The targeted relationship between lncRNA NEAT1 and miR-124-3p was subsequently confirmed by dual-luciferase and co-transfection assays.ResultsMiR-124-3p was identified as a target of NEAT1, and could be negatively regulated by NEAT1 in EC-ESCs. The expression level of NEAT1 was evidently increased, whereas that of miR-124-3p was decreased, in the EM in vivo model, EM tissues and EC-ESCs from patients with EM. The loss-of-function assays further established that silencing of NEAT1 could inhibit EC-ESC proliferation, migration, and invasion, but it led to the promotion of apoptosis via targeting miR-124-3p.ConclusionsNEAT1 is significantly upregulated in EM, promoting malignant behavior in EM through targeting miR-124-3p expression.
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Abstract

Background Endometriosis (EM) is a gynecological disease that poses severe health risks to women, although its pathogenesis has yet to be fully elucidated. It has been shown that long non-coding RNAs (lncRNAs) are closely associated with EM initiation and have a role in the development of this disease. Previous studies exploring the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) have shown that this lncRNA functions as a tumor promoter in endometrial cancer. However, its exact mechanism of action in EM remains unclear.

Objective

This report was designed to illustrate the potential molecular mechanisms of lncRNA NEAT1 on EM.

Methods

Endometrial tissues were extracted from EM model rats and patients with EM. Hematoxylin and eosin staining was applied to detect the morphological changes that occurred in rats after construction of the model. Endometrial stromal cells (ESCs) were extracted from either ectopic endometrium (EC) or eutopic endometrium (EU) tissues from patients with EM. LncRNA NEAT1 and miR-124-3p expression in EM tissues and cells were subsequently evaluated by reverse transcription-quantitative (RT-q)PCR analysis. MTT assay, flow cytometric analysis, western blot assay and Transwell assay were then employed to examine the effect of NEAT1 and miR-124-3p on EC-ESC proliferation, apoptosis, migration and invasion, respectively. The targeted relationship between lncRNA NEAT1 and miR-124-3p was subsequently confirmed by dual-luciferase and co-transfection assays.

Results

MiR-124-3p was identified as a target of NEAT1, and could be negatively regulated by NEAT1 in EC-ESCs. The expression level of NEAT1 was evidently increased, whereas that of miR-124-3p was decreased, in the EM in vivo model, EM tissues and EC-ESCs from patients with EM. The loss-of-function assays further established that silencing of NEAT1 could inhibit EC-ESC proliferation, migration, and invasion, but it led to the promotion of apoptosis via targeting miR-124-3p.

Conclusions

NEAT1 is significantly upregulated in EM, promoting malignant behavior in EM through targeting miR-124-3p expression. Similar content being viewed by others Data availability The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request. Change history 17 July 2025 A Correction to this paper has been published: https://doi.org/10.1007/s13258-025-01651-w

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J Physiol Biochem 75:379–389 Zhang L, Li HH, Yuan M, Li D, Sun C, Wang GY (2020) Serum exosomal microRNAs as potential circulating biomarkers for endometriosis. Dis Markers 2020:2456340 Zondervan KT, Becker CM, Koga K, Missmer SA, Taylor RN, Viganò P (2018) Endometriosis. Nat Rev Dis Primers 4:9 Author information Authors and Affiliations Corresponding author Ethics declarations Conflict of interests Donglan Yuan, Dandan Zhu, Boyu Yin, Hongshan Ge, Yinling Zhao, Aihua Huang, Xiaosu Wang, Xiuhong Cao, Nan Xia and Hua Qian declare that they have no competing interests. Additional information Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. The original article was revised due an error in Figure 4. Supplementary Information Below is the link to the electronic supplementary material. 13258_2021_1184_MOESM1_ESM.tif (download TIF ) Supplementary Figure 1. Typical Papanicolaou smear in tissues from EM rats at different periods (preestrus, estrus, postestrus and interestrus) (TIF 9609 KB) Rights and permissions Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. About this article Cite this article Yuan, D., Zhu, D., Yin, B. et al. Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p. Genes Genom 44, 527–537 (2022). https://doi.org/10.1007/s13258-021-01184-y Received: Accepted: Published: Version of record: Issue date: DOI: https://doi.org/10.1007/s13258-021-01184-y

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endometriosis

MeSH descriptors

Endometriosis Endometriosis MicroRNAs MicroRNAs MicroRNAs RNA, Long Noncoding RNA, Long Noncoding RNA, Long Noncoding Animals Apoptosis Apoptosis Endometrium Endometrium Female Humans Rats

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