Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p
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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References (47)
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Cited by (5)
- Mechanisms of KLF10 in Regulating Proliferation of Endometriotic Stromal Cells in Endometriosis 2025
- Identification of key genes associated with infertile endometriosis based on bioinformatic analysis 2025
- Modulation of Long Non-coding RNA FAS-AS1/FAS/Caspase3 Axis in Endometriosis: A Cross-sectional Study 2024
- Identification of key genes associated with infertile endometriosis based on bioinformatic analysis 2024
- circPLOD2 knockdown suppresses endometriosis progression via the miR-216a-5p/ZEB1 axis 2023
Source provenance
- europepmc
- last seen: 2026-07-26T06:08:39.051465+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-05-13T22:24:03.506079+00:00