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

Abstract

Uterine disease: Regulatory pathways identified A regulatory link between two proteins involved in the progression of a debilitating uterine condition highlights a potential therapeutic target. Adenomyosis involves the invasion of cells from the inner lining of the uterus (the endometrium) into the uterine muscle wall (the myometrium), resulting in heavy, prolonged periods and chronic pain. The aberrent activation of a protein called β-catenin triggers adenomyosis, but the precise mechanisms are unclear. A team led by Jung-Ho Shin at the Korea University Medical Center, Seoul, South Korea, and Jae-Wook Jeong, Michigan State University, Grand Rapids, USA, used sequencing techniques in mice and human tissue samples to identify the pathways governed by β-catenin in adenomyosis. They found that the Tgf-β2 gene is directly regulated by β-catenin in the uterus. TGF-β2 levels were elevated in human adenomyosis lesions, suggesting the protein could be a therapeutic target.