Endometrial epithelial cells-derived exosomes deliver microRNA-30c to block the BCL9/Wnt/CD44 signaling and inhibit cell invasion and migration in ovarian endometriosis

Mengmeng Zhang, Xi Wang, Xiaomeng Xia, Xiaoling Fang, Tingting Zhang, Fengying Huang
Cell death discovery · 2022 · vol. 8(1) · doi:10.1038/s41420-022-00941-6 · W4224262409
article OA: gold CC0 ⤵ 15 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Endometrial epithelial cell-derived exosomes deliver microRNA-30c to block BCL9/Wnt/CD44 signaling, inhibiting cell invasion and migration in ovarian endometriosis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated the role of microRNA-30c (miR-30c) and its target BCL9 in ovarian endometriosis by comparing expression in eutopic vs ectopic endometrial tissues from patients and in ectopic vs eutopic endometrial epithelial cells, and by using isolated endometrial epithelial cell-derived exosomes. The authors found reduced miR-30c and increased BCL9 in ovarian endometriosis tissues and ectopic epithelial cells, and showed that normal endometrial epithelial cell exosomes delivered miR-30c to ectopic cells, suppressing invasion and migration in Transwell and wound-healing assays, with associated EMT marker shifts; they further used a dual-luciferase reporter assay and modulation experiments indicating miR-30c directly targeted BCL9 and inhibited the BCL9/Wnt/β-catenin/CD44 axis. miR-30c-loaded exosomes also reduced metastasis of ectopic nodules in a mouse model. A key limitation is that the study primarily uses in vitro coculture/exosome delivery and in vivo nodule assays without detailing patient-level causal outcomes or broader mechanistic validation beyond the BCL9/Wnt/CD44 pathway. This paper is centrally about endometriosis — specifically, ovarian endometriosis mechanisms where endometrial epithelial exosomes deliver miR-30c to inhibit BCL9/Wnt/CD44 signaling and reduce ectopic cell invasion/migration.

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Abstract

Abstract Endometriosis (EMs) is a benign gynecological disorder showing some tumor-like migratory and invasive phenotypes. This study intended to investigate the role of microRNA-30c (miR-30c) in EMs, which is involved with B-cell lymphoma 9 (BCL9), an activator of the Wnt/β-catenin signaling pathway. EMs specimens were clinically collected for determination of miR-30c and BCL9 expression. Exosomes were isolated from endometrial epithelial cells (EECs), and the uptake of exosomes by ectopic EECs (ecto-EECs) was characterized using fluorescence staining and confocal microscopy. The binding of miR-30c to BCL9 was validated by dual-luciferase reporter assay. Artificial modulation (up- and down-regulation) of the miR-30c/BCL9/Wnt/CD44 regulatory cascade was performed to evaluate its effect on ecto-EEC invasion and migration, as detected by Transwell and wound healing assays. A mouse model of EMs was further established for in vivo substantiation. Reduced miR-30c expression and elevated BCL9 expression was revealed in EMs ectopic tissues and ecto-EECs. Normal EECs-derived exosomes delivered miR-30c to ecto-EECs to suppress their invasive and migratory potentials. Then, miR-30c was observed to inhibit biological behaviors of ecto-EECs by targeting BCL9, and the miR-30c-induced inhibitory effect was reversed by BCL9 overexpression. Further, miR-30c diminished the invasion and migration of ecto-EECs by blocking the BCL9/Wnt/CD44 axis. Moreover, miR-30c-loaded exosomes attenuated the metastasis of ecto-EEC ectopic nodules. miR-30c delivered by EECs-derived exosomes repressed BCL9 expression to block the Wnt/β-catenin signaling pathway, thus attenuating the tumor-like behaviors of ecto-EECs in EMs.

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endometriosis

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