ArticleBMC women's health2026
HAGLR promotes endometriosis progression via the miR-185-5p/VEGFA axis and serves as a potential diagnostic biomarker.
Article in BMC women's health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundEndometriosis (EMs) is a prevalent gynecological disorder among women of reproductive age. HAGLR has recently been identified as a potential factor in EMs, but its functional role and underlying mechanisms remain unclear.
methods110 EMs patients and 110 controls were enrolled. The abundance of HAGLR, miR-185-5p, and VEGFA were quantified by qRT-PCR. Pearson correlation, ROC curve analysis, and logistic regression were performed to estimate clinical associations, diagnostic value, and risk factors. Cell proliferation was assessed using the CCK-8 assay, while migration and invasion were examined via Transwell assays. Regulatory interactions were predicted through bioinformatics and validated via dual-luciferase reporter assays and rescue experiments.
resultsHAGLR expression was significantly elevated in EMs tissues and identified as an independent risk factor with good diagnostic performance for EMs. High HAGLR expression was associated with deep infiltrating endometriosis (DIE) and advanced rASRM stages. Functional assays showed that HAGLR knockdown suppressed proliferation, migration, and invasion of 12Z cells. Mechanistically, HAGLR acted as a molecular sponge for miR-185-5p, as evidenced by their negative correlation. miR-185-5p directly targeted VEGFA, which was found to be upregulated in EMs and positively correlated with HAGLR expression. VEGFA overexpression rescued the inhibitory effects of HAGLR silencing, restoring cell growth and invasiveness.
conclusionsHAGLR may be a potential, valuable diagnostic biomarker and therapeutic candidate in EMs. These findings reveal that HAGLR promotes EMs progression by modulating the miR-185-5p/VEGFA axis, contributing to enhanced proliferation and invasion of endometrial stromal cells.
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