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β-catenin activates TGF-β-induced epithelial?mesenchymal transition in adenomyosis

Experimental & Molecular Medicine 2020년 52권 10호 p.6 ~ 6
유정윤, 구본정, 김태훈, Ahn Jong-Il, 안지연, Yang Woo-Sub, 임정묵, Taketo Maketo M., 신중호, 정재욱,
소속 상세정보
유정윤 ( Yoo Jung-Yoon ) - Yonsei University Collgeg of Medicine Department of Biochemistry and Molecular Biology
구본정 ( Ku Bon-Jeong ) - Chungnam National University College of Medicine Department of Internal Medicine
김태훈 ( Kim Tae-Hoon ) - Michigan State University Department of Obstetrics, Gynecology and Reproductive Biology
 ( Ahn Jong-Il ) - Seoul National University Department of Agricultural Biotechnology
안지연 ( Ahn Ji-Yeon ) - Seoul National University Research Institutes of Agriculture and Life Sciences
 ( Yang Woo-Sub ) - Seoul National University Department of Agricultural Biotechnology
임정묵 ( Lim Jeong-Mook ) - Seoul National University Department of Agricultural Biotechnology
 ( Taketo Maketo M. ) - Kyoto University Graduate School of Medicine Division of Experimental Therapeutics
신중호 ( Shin Jung-Ho ) - Korea University Guro Hospital Department of Obstetrics and Gynecology
정재욱 ( Jeong Jae-Wook ) - Michigan State University Department of Obstetrics, Gynecology and Reproductive Biology

Abstract


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.

키워드

Gene regulation; Urogenital reproductive disorders

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