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Sci Rep. 2019 Dec 27;9(1):20056. doi: 10.1038/s41598-019-56302-4.

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

Author information

1
Department of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Oita, Japan. tomokoh@oita-u.ac.jp.
2
Department of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Oita, Japan.
3
Division of Obstetrics and Gynecology, Support System for Community Medicine, Faculty of Medicine, Oita University, Oita, Japan.
4
Translational Chemical Biology Laboratory, Faculty of Medicine, Oita University, Oita, Japan.
5
Department of Clinical Pharmacology and Therapeutics, Faculty of Medicine, Oita University, Oita, Japan.

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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