Mechanisms of KLF10 in Regulating Proliferation of Endometriotic Stromal Cells in Endometriosis
article
OA: closed
CC0
AI-generated summary
KLF10 inhibits endometriotic stromal cell proliferation by transcriptionally upregulating miR-200c-3p, which reduces NEAT1 expression.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
Abstract
OBJECTIVES: Endometriotic stromal cells (ESCs) are extensively found in endometriosis (EM). This study aims to investigate the effects and regulatory mechanisms of KLF10 on the proliferation of ESCs in EM. METHODS: Human ESCs from eutopic and ectopic endometrium were isolated and identified. Levels of KLF10, miR-200c-3p, and lncRNA NEAT1 in cells were detected by reverse transcription-quantitative polymerase chain reaction and Western blot analysis. Expression of KLF10, miR-200c-3p, and NEAT1 were silenced in ectopic ESCs, followed by an assessment of cell proliferation. Chromatin immunoprecipitation and dual-luciferase reporter assays were conducted to analyze the binding of KLF10 to the miR-200c-3p promoter. RNA immunoprecipitation and dual-luciferase reporter assays were performed to analyze the interaction between miR-200c-3p and NEAT1. NEAT1 RNA stability was measured. RESULTS: Compared to Eut-ESCs, Ect-ESCs exhibited decreased KLF10 and miR-200c-3p expression and increased NEAT1 expression. Overexpression of KLF10 inhibited the proliferation of Ect-ESCs. Mechanistically, KLF10 transcriptionally promoted miR-200c-3p expression, reducing the binding of miR-200c-3p to NEAT1 and downregulating NEAT1 expression. Combined experimental results showed that miR-200c-3p downregulation or NEAT1 overexpression could alleviate the inhibitory effect of KLF10 overexpression on the proliferation of Ect-ESCs. LIMITATIONS: We only investigated the function of KLF10 in Ect-ESC proliferation of EM on the cellular level, but the effect of KLF10 on abnormal Ect-ESC migration and invasion remains to be explored. Besides, there is no interference experiments performed on Eut-ESCs, and no animal experiment was included. CONCLUSIONS: KLF10 transcriptionally promoted miR-200c-3p expression reduced the binding of miR-200c-3p to NEAT1, thus downregulating NEAT1 expression and inhibiting the proliferation of Ect-ESCs.
My notes (saved in your browser only)
Condition tags
MeSH descriptors
Citation neighborhood
Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.
References (26)
- Autophagy contributes to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis† via openalex
- Biomarkers in endometriosis: challenges and opportunities via openalex
- Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis via openalex
- Clinical Management of Endometriosis via openalex
- Endometriosis via openalex
- Endometriosis, infertility and MicroRNA's: A review via openalex
- Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p via openalex
- Host immunity and KLF 11 deficiency together promote fibrosis in a mouse model of endometriosis. via openalex
- Integrated Bioinformatics Analysis Reveals Function and Regulatory Network of miR‐200b‐3p in Endometriosis via openalex
- Metformin Inhibits the Estrogen-mediated Epithelial-Mesenchymal Transition of Ectopic Endometrial Stromal Cells in Endometriosis via openalex
- miR-200c suppresses endometriosis by targeting MALAT1 in vitro and in vivo via openalex
- Resveratrol impairs cellular mechanisms associated with the pathogenesis of endometriosis via openalex
- The Pathological Role of miRNAs in Endometriosis via openalex
- Upregulation of HTRA1 mediated by the lncRNA NEAT1/miR-141-3p axis contributes to endometriosis development through activating NLRP3 inflammasome-mediated pyroptotic cell death and cellular inflammation via openalex
- W4388948152 via openalex
- W2263276115 via openalex
- W2490109341 via openalex
- W2605821181 via openalex
- W3016482991 via openalex
- W3026854910 via openalex
- W3128842362 via openalex
- W3134885188 via openalex
- W4285908245 via openalex
- W4310157165 via openalex
- W4310995147 via openalex
- W2144357057 via openalex
Source provenance
- europepmc
- last seen: 2026-06-04T01:30:01.192114+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-05-27T00:31:19.326749+00:00
License: CC0
· commercial use OK