β-catenin signaling inhibitors ICG-001 and C-82 improve fibrosis in preclinical models of endometriosis

Tomoko Hirakawa, Kaei Nasu, Saori Miyabe, Hiroyuki Kouji, Akira Katoh, Naoto Uemura, Hisashi Narahara
Scientific reports · 2019 · vol. 9(1) , pp. 20056 · doi:10.1038/s41598-019-56302-4 · PMID:31882904 · W2997653787
article OA: gold CC0 ⤵ 7 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

CBP/β-catenin signaling inhibitors ICG-001 and C-82 reduced fibrosis, proliferation, and migration while promoting apoptosis in endometriosis stromal cells and ICG-001 decreased lesion growth in a mouse model.

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

This study assessed whether CBP/β-catenin signaling contributes to endometriosis-associated fibrosis by comparing β-catenin expression and testing the CBP/β-catenin inhibitors ICG-001 and C-82 in endometriotic cyst stromal cells (ECSC) versus normal endometrial stromal cells (NESC), with ICG-001 also evaluated in a mouse endometriosis model. β-catenin protein was higher in ECSC than in NESC, and both inhibitors reduced ECSC proliferation, fibrogenic behavior (α-SMA mRNA), migration, and 3D gel contractility while increasing apoptosis; in mice, ICG-001 reduced the number of endometriotic lesions, with decreased fibrosis by collagen and α-SMA staining. A major caveat was that two ICG-001–treated mice died after injection, attributed to excess bleeding, potentially limiting interpretation of in vivo tolerability-related effects. This paper is centrally about endometriosis — it tests CBP/β-catenin signaling inhibition (ICG-001, C-82) to attenuate endometriotic lesion growth and fibrosis in vitro and in vivo.

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Abstract

Endometriosis exhibits unique characteristics, such as fibrosis, resistance to apoptosis, and promotion of cell proliferation; however, its pathophysiology is not fully understood. Recurrence rates after treatment are high, and the progression risk continues until menopause; hence, more effective therapy for endometriosis is needed. CREB-binding protein (CBP)/β-catenin signaling inhibitors have demonstrated antifibrogenetic effects in liver, lung, and skin diseases. The present study evaluated the effects of two CBP/β-catenin signaling inhibitors, ICG-001 and C-82, on the progression of endometriosis using endometriotic cyst stromal cells from the ovary and normal endometrial stromal cells from the uterus. ICG-001 was also evaluated in a mouse model. ICG-001 and C-82 inhibited cell proliferation, fibrogenesis, and cell migration, and promoted apoptosis in vitro. ICG-001 inhibited the growth of endometriotic lesions in the mouse model. CBP/β-catenin signaling plays an important role in the pathophysiology of endometriosis. Inhibiting the CBP/β-catenin signal can be a therapeutic target for endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

beta Catenin Bridged Bicyclo Compounds, Heterocyclic Endometriosis Heterocyclic Compounds, 2-Ring Piperazines Pyrimidinones Signal Transduction Animals beta Catenin beta Catenin Bridged Bicyclo Compounds, Heterocyclic Disease Models, Animal Endometriosis Female Heterocyclic Compounds, 2-Ring Humans Mice Piperazines Pyrimidinones Signal Transduction

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