Study on the role of miR-433-3p in the occurrence and development of endometriosis

Lulu Wang, Wang L, Bai J, Jing Bai, Xiaoqing Zhu, Zhu X
Nucleosides, nucleotides & nucleic acids · 2026 · pp. 1–16 · doi:10.1080/15257770.2026.2718818 · PMID:42627080 · W7203946303
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This study found that miR-433-3p is downregulated in endometriosis, serves as a diagnostic biomarker, and inhibits endometrial stromal cell proliferation and invasion by targeting CHL1.

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Abstract

This study aims to characterize the expression pattern and biological functions of miR-433-3p in endometriosis. Eutopic and ectopic endometrial tissues were collected from endometriosis patients, and the expression level of miR-433-3p was detected by RT-qPCR. Serum samples were also collected from endometriosis patients and healthy female controls, and the diagnostic value of miR-433-3p for endometriosis was evaluated by receiver operating characteristic curve. In cell experiments, CCK-8 and Transwell assays were performed to assess the effects of miR-433-3p on the proliferation, migration and invasion of endometrial stromal cells (ESCs). RT-qPCR was used to detect the expression levels of epithelial-mesenchymal transition (EMT) markers. A dual-luciferase reporter assay was conducted to verify the targeted binding relationship between miR-433-3p and CHL1. The results showed that the level of miR-433-3p in ectopic endometrium was significantly lower than that in eutopic endometrium. Moreover, circulating miR-433-3p levels in the serum of endometriosis patients were significantly lower than those in healthy controls. Serum miR-433-3p demonstrated excellent diagnostic efficacy for endometriosis, with an AUC of 0.8777, a sensitivity of 93.90%, and a specificity of 76.25%. In cells, overexpression of miR-433-3p significantly suppressed the proliferation, migration, invasion and EMT. Mechanistically, CHL1 was identified as a direct downstream target of miR-433-3p, and rescue experiments confirmed that restored CHL1 expression could partially reverse the inhibitory effect of miR-433-3p on the aggressive biological phenotype of ESCs. Based on the above research results, we propose the following hypothesis: In endometriosis, miR-433-3p may inhibit the proliferation and invasion of ESCs by targeting CHL1. Moreover, circulating miR-433-3p is expected to become a non-invasive candidate biomarker for endometriosis.

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