ArticleResearch square2025
Polychlorinated Biphenyl-126 Activates AXL/ERb/DNMT3A Axis to Drive Endometriosis Progression.
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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
9 authors.
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Abstract
Endometriosis is a pathological condition in which endometrial cells proliferate outside the uterine cavity, resulting in pelvic pain and infertility. Exposure to endocrine-disrupting chemicals (EDCs) has been implicated in the progression of endometriosis, though the precise mechanisms remain largely undefined. Among EDCs, elevated levels of polychlorinated biphenyl (PCB)-126 have been strongly associated with endometriosis, particularly in patients with deep infiltrating disease. 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 key driver of disease progression. PCB-126 also enhanced ERβ activity via upregulation of the AXL Receptor Tyrosine Kinase (AXL)/Growth Arrest-Specific 6 (GAS6) signaling pathway in endometriotic lesions. Notably, BMS-777607, an AXL inhibitor, effectively suppressed lesion growth in this model. Moreover, the PCB-126/ERβ axis directly increased expression of DNA Methyltransferase 3A (DNMT3A), contributing to inflammation and immune dysregulation in endometriotic tissue. Collectively, these findings suggest that PCB-126 promotes endometriosis progression through coordinated activation of the AXL/ERβ/DNMT3A axis, driving estrogen-mediated epigenetic and immunoinflammatory responses.
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