Abstract: Adenomyosis (ADS) is a common benign gynecological disorder characterized by the invasion of endometrial glands and stroma into the myometrial wall, which may result in uterine focal or diffuse enlargement. However, the pathogenesis of ADS has not been illuminated yet. Currently, most researchers think that abnormal proliferation of the basal endometrial cells and their invasion to the myometrium are the leading cause of adenomyosis. Whereas, the precise factors that induce to the aberrant invasion of endometrium are still unknown. During the process of epithelial-mesenchymal transition (EMT), epithelial cells lost cell polarity, and cell tight junction and adhesive junction both weaken. They acquire infiltration and migration ability and become cells like mesenchymal cells. EMT induces cell migration and infiltration during tumorgenesis. The biological behavior of endometrial cells invading myometrium of ADS is very similar to the EMT. It has been demonstrated that EMT plays an important role in the development of ADS. As for the clinical treatment of ADS is facing many challenges, illuminating the pathogenesis of ADS would be the key to explore an effective way for prevention and treatment of ADS.

Key words: Adenomyosis, Epithelial-mesenchymal transition, Endometrium, Cell proliferation, Fibrosis