Study on the role of miR-146b-3p in the occurrence and development of endometriosis

Yan Zhang, Y. Zhang, D W Han
In: Turkish Journal of Biochemistry · 2025 · doi:10.1515/tjb-2025-0222 · W4415267760
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This study found that miR-146b-3p is elevated in endometriosis and promotes disease progression by targeting UNC5C, influencing cell proliferation, apoptosis, migration, invasion, and inflammatory responses.

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Abstract

Abstract Objectives A chronic inflammatory disease, endometriosis is recognized by the ectopic tissue growth of endometrium, but its pathogenesis has not been fully elucidated. Recently, miRNAs have been identified as a key regulator in the pathological process of endometriosis. This study investigated the function and molecular mechanism of miR-146b-3p in the occurrence and development of endometriosis. Methods In this study, 90 patients with endometriosis and 90 age-matched patients who had surgery for uterine fibroids or simple ovarian cysts were selected for the research objects. miR-146b-3p and UNC5C levels were examined by qRT-PCR in clinical endometriotic tissues and normal tissues. The impact of miR-146b-3p on endometriotic cells was verified through transfection of miR-146b-3p mimic or inhibitor. Apoptosis and proliferation were detected using flow cytometry and CCK8 assay. Transwell method was employed for examination of cell migration and invasion. The interaction of miR-146b-3p and UNC5C was detected via luciferase activity. Results miR-146b-3p levels were significantly elevated in endometriotic tissues and gradually raised with increasing rASRM grade. In endometriotic cells, up-regulation of miR-146b-3p inhibited apoptosis, facilitated cell proliferation, migration and invasion, and elevated IL-6 and TNF-α, whereas downregulation of miR-146b-3p exhibited opposite trend. In addition, miR-146b-3p targeted UNC5C, which altered the influences of miR-146b-3p on apoptosis, proliferation, migration, invasion, and inflammatory responses. Conclusions This study found that miR-146b-3p regulates inflammatory response and progression of endometriosis by targeting UNC5C, which provided a theoretical basis for the exploitation of new diagnostic biomarkers or searching for potential therapeutic targets.

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Outcome instruments

rASRM

Condition tags

endometriosis

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (28)

Source provenance

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