Yang Chaoyi, Wang Shujun, Li Mengru, Pang Xiangli, Tan Aili
Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, Hubei.
Eur J Histochem. 2025 Jun 17;69(3). doi: 10.4081/ejh.2025.4176.
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.
子宫内膜异位症是一种具有与肿瘤相似特征的良性疾病。最近的研究发现，促红细胞生成素产生性肝癌受体A2（EphA2）具有促进肿瘤和抑制肿瘤的双重作用。本研究的目的是探讨EphA2在子宫内膜异位症中的具体调控机制。采用生物信息学方法分析子宫内膜异位症中Eph蛋白家族的表达水平。在临床水平上，运用qPCR、蛋白质免疫印迹法和免疫组织化学法来验证EphA2水平升高与子宫内膜异位症之间的相关性。在体外探究阻断EphA2对原发性在位子宫内膜间质细胞的迁移、侵袭、增殖和凋亡的影响。我们的研究表明，子宫内膜异位症患者中EphA2表达升高，体外阻断EphA2通过AMPK信号通路抑制细胞增殖、迁移和侵袭。靶向EphA2可通过AMPK信号通路抑制子宫内膜异位症的进展。
