High-Expression of Neuropilin 1 Correlates to Estrogen-Induced Epithelial-Mesenchymal Transition of Endometrial Cells in Adenomyosis

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AI-generated summary by claude@2026-06+body, 2026-06-06

Neuropilin 1 is significantly increased in adenomyosis endometrium and promotes estrogen-induced epithelial-mesenchymal transition and migration in endometrial cells.

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AI-generated deep summary by claude@2026-06, 2026-06-06

The paper investigates whether neuropilin 1 (NRP1) contributes to estrogen-induced epithelial-mesenchymal transition (EMT) during adenomyosis, focusing on its expression in human adenomyosis endometrium and its functional effects in endometrial cells. Using endometrial samples, the authors report that NRP1 expression is significantly increased in adenomyosis endometrium, especially in ectopic tissue, and in human endometrial cells (HEC-1-A) NRP1 overexpression drives a mesenchymal phenotype with reduced E-cadherin and occludin, increased α-SMA and N-cadherin, and enhanced migration. They further show that 17β-estradiol up-regulates NRP1 dose-dependently, an effect blocked by the estrogen receptor inhibitor raloxifene, while NRP1 knockdown suppresses E2-induced EMT and reduces Smad3 phosphorylation with restoration of Slug and Snail1 mRNA. A key limitation is the mechanistic evidence is largely derived from in vitro cell models rather than in vivo validation. This paper is centrally about endometriosis and/or adenomyosis—adenomyosis specifically—linking high NRP1 expression and estrogen-driven EMT of endometrial cells to adenomyosis pathogenesis.

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Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Endometrium Epithelial-Mesenchymal Transition Estradiol Neuropilin-1 Adenomyosis Adult Antigens, CD Antigens, CD Cadherins Cadherins Cell Line Dose-Response Relationship, Drug Endometrium Endometrium Epithelial-Mesenchymal Transition Estradiol Female Humans Middle Aged

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europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
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pubmed
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License: CC0 · commercial use OK