AURKA enhances the glycolysis and development of ovarian endometriosis through ERβ

Abstract

Ovarian endometriosis is a benign, estrogen-dependent gynecological disorder. Estrogen receptor beta (ERβ), a nuclear receptor for estradiol, plays an important role in the development of ovarian endometriosis. Here, we investigated the biological significance of Aurora kinase A (AURKA) in ovarian endometriosis and the mechanism by which it regulated ERβ. We used immunohistochemical assays to verify that AURKA and ERβ were highly expressed in ectopic endometrial tissues. Cell proliferation and colony formation assays were used to demonstrate that AURKA promoted the proliferation of endometriosis cells. Wound healing assay, Transwell migration assay and Matrigel invasion assay further show that AURKA enhanced ability of endometriosis cells to migrate and invade. In addition, AURKA was shown to stimulate glycolysis in endometriosis cells by measuring the concentration of glucose and lactate in the cell supernatants. Moreover, the AURKA inhibitor Alisertib was found to inhibit the progression of ovarian endometriosis and glycolysis in a mouse model of endometriosis by measuring ectopic tissues as well as by testing the peritoneal fluid of mice. Furthermore, Co-immunoprecipitation assay showed that AURKA interacted with ERβ. The rescue experiments confirmed that AURKA regulated the development and glycolysis of ovarian endometriosis in an ERβ-dependent manner. In conclusion, AURKA contributed to the development of ovarian endometriosis by upregulating of ERβ. AURKA may represent a new target for the treatment of ovarian endometriosis.