ArticleResearch square2025
Polychlorinated biphenyl Endocrine Disruptor Alters Estrogen Receptor beta-Mediated Epigenetic Regulation, Promoting Endometriosis.
Article in Research square, 2025. 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
Background: Endometriosis is a pathological condition characterized by the ectopic proliferation of endometrial cells, resulting in chronic pelvic pain and infertility. Exposure to endocrine-disrupting chemicals (EDCs) has been implicated in the development and progression of endometriosis; however, the underlying mechanisms remain largely unclear. Among these EDCs, elevated levels of polychlorinated biphenyl-126 (PCB-126) have been strongly associated with endometriosis. Yet, how PCB-126 exposure contributes to disease progression remains an unresolved and fundamental question. Method: Surgically induced endometriosis mice were randomly assigned to treatment with PCB-126 or vehicle control. To assess the effects of PCB-126 on human endometrial cells, immortalized human endometrial epithelial and stromal cell lines were utilized. To investigate the role of AXL receptor tyrosine kinase (AXL) in PCB-126-mediated endometriosis progression, surgically induced endometriosis mice were randomly treated with an AXL inhibitor. To evaluate the contribution of DNA methyltransferase 3A (DNMT3A) to endometriosis progression, ectopic lesions were generated using endometrium-specific Dnmt3a knockout mice (Dnmt3a Results: In a mouse model of endometriosis, PCB-126 exposure significantly promoted the growth of ectopic lesions by activating the Steroid Receptor Coactivator-1 (SRC-1) isoform/Matrix Metalloproteinase-9 (MMP9)/Estrogen Receptor-β (ERβ) axis, a critical pathway driving disease progression. Additionally, PCB-126 enhanced ERβ activity through upregulation of the AXL/Growth Arrest-Specific 6 (GAS6) signaling pathway within endometriotic lesions. Notably, treatment with BMS-777607, an AXL inhibitor, effectively suppressed ectopic lesion growth in mice. Furthermore, the PCB-126/ERβ axis upregulated Conclusion: PCB-126 promotes endometriosis progression through coordinated activation of the AXL/ERβ/DNMT3A axis, disrupting estrogen-mediated epigenetic regulation and inducing endometriosis-associated immunoinflammatory responses.
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