Mechanisms of KLF10 in Regulating Proliferation of Endometriotic Stromal Cells in Endometriosis

作者：Bo Xia, Yang Liu, Jing Li, Shan Jiang · 发表于：Gynecologic and Obstetric Investigation · 年份：2025 · DOI：10.1159/000546836 · 被引用次数：2 · 研究领域：Endometriosis Research and Treatment、Kruppel-like factors research、Reproductive System and Pregnancy

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 proliferati...