Overexpression of TGF‑β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway

Abstract

Endometriosis is a common gynecological disease with manifestations of endometrial-like tissue outside the uterus. Transforming growth factor-beta (TGF-beta) is known to facilitate a series of biological events in many cells, including migration. However, the roles of TGF-beta in endometriosis still remain largely unknown. The aim of the present study was to discover the role of TGF-beta1 in endometriosis development and progression and its associated mechanisms. It was demonstrated that the expression of TGF-beta1 was significantly elevated in endometriosis in comparison with that in normal tissue. Overexpression of TGF-beta increased the proliferation and upregulated proliferating cell nuclear antigen and cyclin D1 in endometrial stromal cells (ESCs). Furthermore, TGF-beta overexpression also triggered a series of biological events occurring in ESCs, including cell migration and invasion, and activated the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling pathway. The inhibition of the ERK/MAPK pathway reversed the previous effects of TGF-beta overexpression. Collectively, the present results indicate that overexpression of TGF-beta enhances the migration and invasion of ectopic ESCs via the ERK/MAPK signaling pathway, providing theoretical evidence for the development of new treatment methods targeting the TGF-beta-ERK/MAPK signaling pathway for prophylaxis of endometriosis.