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KMID : 0620920200520101754
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Experimental & Molecular Medicine
2020 Volume.52 No. 10 p.1754 ~ p.1765
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β-catenin activates TGF-β-induced epithelial-mesenchymal transition in adenomyosis
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Yoo Jung-Yoon
Ku Bon-Jeong
Kim Tae-Hoon
Ahn Jong-Il
Ahn Ji-Yeon
Yang Woo-Sub
Lim Jeong-Mook
Taketo Maketo M.
Shin Jung-Ho
Jeong Jae-Wook
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Abstract
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Adenomyosis is defined as the presence of ectopic nests of endometrial glands and stroma within the myometrium. Adenomyosis is a common cause of dysmenorrhea, menorrhagia, and chronic pelvic pain but is often underdiagnosed. Despite its prevalence and severity of symptoms, its pathogenesis and etiology are poorly understood. Our previous study showed that aberrant activation of β-catenin results in adenomyosis through epithelial?mesenchymal transition. Using transcriptomic and ChIP-seq analysis, we identified activation of TGF-β signaling in the uteri of mutant mice that expressed dominant stabilized β-catenin in the uterus. There was a strong positive correlation between β-catenin and TGF-β2 proteins in women with adenomyosis. Furthermore, treatment with pirfenidone, a TGF-β inhibitor, increased E-cadherin expression and reduced cell invasiveness in Ishikawa cells with nuclear β-catenin. Our results suggest that β-catenin activates TGF-β-induced epithelial?mesenchymal transition in adenomyosis. This finding describes the molecular pathogenesis of adenomyosis and the use of TGF-β as a potential therapeutic target for adenomyosis.
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KEYWORD
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Gene regulation, Urogenital reproductive disorders
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