ArticleGenes & genomics2022
Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p.
Article in Genes & genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Long non-coding RNA NEAT1 promotes ovarian granulosa cell proliferation and cell cycle progression via the miR-29a-3p/IGF1 axis.Journal of ovarian research · 2025Article
- Identification of key genes associated with infertile endometriosis based on bioinformatic analysis.Frontiers in genetics · 2025Article
- Dysregulated miR-124-3p in endometrial epithelial cells reduces endometrial receptivity by altering polarity and adhesion.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Function of microRNA‑124 in the pathogenesis of cancer (Review).International journal of oncology · 2024Review
- Emerging roles of the long non-coding RNA NEAT1 in gynecologic cancers.Journal of cell communication and signaling · 2023Review
- Regulation of the Key Epithelial Cancer Suppressor miR-124 Function by Competing Endogenous RNAs.International journal of molecular sciences · 2022Review
- Gene expression analysis in endometriosis: Immunopathology insights, transcription factors and therapeutic targets.Frontiers in immunology · 2022Article
- Modulation of Long Non-coding RNA FAS-AS1/FAS/Caspase3 Axis in Endometriosis: A Cross-sectional Study.Journal of human reproductive sciencesArticle
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.