Targeting EphA2 suppresses the proliferation, migration and invasion of endometriosis via the AMPK signaling pathway.

Abstract

Endometriosis is a benign disease with similar characteristics to tumors. Recent studies have found that the erythropoietin-producing hepatoma receptor A2 (EphA2) has the dual effect of promoting tumor and inhibiting tumor. The objective of this study was to explore the specific regulatory mechanism of EphA2 in endometriosis. The expression level of Eph protein family in endometriosis was analyzed by bioinformatics method. At the clinical level, qPCR, Western blot and immunohistochemistry were used to verify the correlation between increased EphA2 levels and endometriosis. The effects of blocking EphA2 on cell migration, invasion, proliferation and apoptosis of primary eutopic endometriotic stromal cells were explored in vitro. Our study indicated that EphA2 expression was elevated in endometriosis patients, and blocking EphA2 in vitro inhibited cell proliferation, migration and invasion through AMPK signaling pathway. Targeting EphA2 can inhibit the progression of endometriosis through the AMPK signaling pathway.