Role of Epithelial-Mesenchymal Transition in Human Adenomyosis: A New Insight into Its Pathogenesis
Hepatocyte growth factor and estrogen induce epithelial-mesenchymal transition by regulating SLUG/SNAIL expression in human adenomyosis.
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This chapter investigates whether hepatocyte growth factor (HGF) and estrogen promote epithelial-mesenchymal transition (EMT) as a mechanism underlying gland invagination in human adenomyosis. Biopsy specimens spanning endometrium to myometrium were collected after hysterectomy from women with and without adenomyosis, and the relationship between HGF and E-cadherin/N-cadherin was assessed by qRT-PCR and immunohistochemistry; mechanistic experiments used Ishikawa cells to examine SLUG and SNAIL expression under HGF and estrogen, including inhibition with anti-HGF antibody or an estrogen receptor antagonist. The authors report that HGF downregulated E-cadherin and upregulated N-cadherin in endometrial epithelial cells, with an inverse HGF–E-cadherin relationship in basalis endometrium from women with adenomyosis, and that HGF plus estrogen increased SLUG/SNAIL expression additively, which was abrogated by pathway inhibition; they also observed HGF-induced morphological changes and migration. The paper acknowledges adenomyosis pathogenesis remains elusive and frames its findings as mechanistic support for the accepted gland invagination concept. This paper is centrally about endometriosis and/or adenomyosis — specifically, it focuses on EMT driven by HGF and estrogen in human adenomyosis.
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References (28)
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