miR-21 regulates autophagy and apoptosis of ectopic endometrial stromal cells of adenomyosis via PI3K/ AKT/ mTOR pathway.

Adenomyosis (AM) is a common and challenging disease in gynecological clinics, which adversely affects women's physical and mental health. Despite the growing number of studies, the mechanisms associated with the growth of the lesion are poorly understood. Studies show that abnormal proliferation, apoptosis, and migration in ectopic endometrial stromal cells (EESc) of AM may contribute to the development and progression of AM. Understanding the underlying molecular mechanisms can significantly contribute to diagnosing and treating AM. In the present study, EESc was isolated and cultured from the ectopic endometrium of patients with AM. These cells were treated with a PI3K/AKT activator (740 Y-P) and an inhibitor (LY294002), while the expression of microRNA-21 (miR-21) was interfered with. The effects of miR-21 on the apoptosis and autophagy of EESc, as well as the associated mechanisms, were investigated from multiple perspectives. Here, we found that 740 Y-P could significantly promote proliferation, inhibit apoptosis of EESc, and increase the expression of mTOR and p-mTOR proteins in EESc. Moreover, activating miR-21 enhanced the pro-migration effect of 740 Y-P and reversed the pro-apoptotic effect of LY294002, reducing the apoptosis rate and increasing the migration ability of EESc. Our investigation revealed that miR-21 can inhibit apoptosis and autophagy and promote migration of EESc. This effect is likely mediated via the PI3K/AKT/mTOR pathway.