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

Jung-Yoon Yoo, Jung‐Yoon Yoo, Bon Jeong Ku, Tae Hoon Kim, Jong Il Ahn, Ji Yeon Ahn, Woo Sub Yang, Jeong Mook Lim, Maketo M Taketo, Jung‐Ho Shin, Jung-Ho Shin, Jae‐Wook Jeong
Experimental & molecular medicine · 2020 · vol. 52(10) , pp. 1754–1765 · doi:10.1038/s12276-020-00514-6 · PMID:33060769 · PMC8080580 · W3092718736
article OA: gold CC0 ⤵ 15 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that β-catenin activates TGF-β-induced epithelial-mesenchymal transition, identifying a molecular mechanism and potential therapeutic target for adenomyosis.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated how aberrant β-catenin activation contributes to adenomyosis by combining transcriptomic profiling and ChIP-seq in a mouse uterine model (Pgrcre/+Ctnnb1f(ex3)/+) and by analyzing human adenomyosis tissues and matched eutopic endometrium. The authors identified TGF-β signaling activation, including direct regulation of Tgf-β2 by activated β-catenin in mice, and found a strong positive correlation between β-catenin and TGF-β2 protein levels in women with adenomyosis; in cultured Ishikawa cells with nuclear β-catenin, the TGF-β inhibitor pirfenidone increased E-cadherin and reduced invasiveness. A major caveat is that key mechanistic inference depends on associations and on a single inhibitor/cell model, with in vivo TGF-β pathway activity characterized at early time points (1 month of age) in pooled samples. This paper is centrally about endometriosis and/or adenomyosis — specifically adenomyosis, focusing on β-catenin–TGF-β2–driven epithelial–mesenchymal transition in adenomyotic lesions.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

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.

My notes (saved in your browser only)

Condition tags

adenomyosischronic_pelvic_paindysmenorrhea

MeSH descriptors

Adenomyosis beta Catenin Disease Susceptibility Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition Transforming Growth Factor beta Adenomyosis Adenomyosis Adenomyosis Animals beta Catenin Binding Sites Cadherins Cadherins Disease Models, Animal Fluorescent Antibody Technique Gene Expression Regulation Humans Immunohistochemistry Mice

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (66)

Cited by (16)

Source provenance

europepmc
last seen: 2026-06-23T06:15:44.889181+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:21:36.268089+00:00
License: CC0 · commercial use OK