AURKA Enhances the Glycolysis and Development of Ovarian Endometriosis Through ERβ
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Aurora kinase A promotes ovarian endometriosis development and glycolysis by interacting with and upregulating estrogen receptor beta.
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Abstract
Ovarian endometriosis (EMs) 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 EMs. Here, we investigated the biological significance of aurora kinase A (AURKA) in ovarian EMs and the mechanism by which it regulates 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 EMs cells. Wound-healing assay, Transwell migration assay, and Matrigel invasion assay further showed that AURKA enhanced the ability of EMs cells to migrate and invade. In addition, AURKA was shown to stimulate glycolysis in EMs 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 EMs and glycolysis in a mouse model of EMs by measuring ectopic tissues as well as by testing the peritoneal fluid of mice. Furthermore, coimmunoprecipitation assay showed that AURKA interacted with ERβ. The rescue experiments confirmed that AURKA regulated the development and glycolysis of ovarian EMs in an ERβ-dependent manner. AURKA contributed to the development of ovarian EMs by upregulating of ERβ. AURKA may represent a new target for the treatment of ovarian EMs.
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Cited by (11)
- Aberrant mitochondria in endometriosis: From pathogenic mechanisms to therapeutic opportunities 2026
- PRMT3-mediated FOXO1 arginine methylation exacerbates oxidative stress-induced decidualization defects in the eutopic endometrium of endometriosis 2025
- AlkB Homolog 5 Regulates Hexokinase 2-Mediated Glycolysis and Participates in the Progression of Endometriosis 2025
- Warburg-like Metabolic Reprogramming in Endometriosis: From Molecular Mechanisms to Therapeutic Approaches 2025
- Clear Cell Carcinoma Caused by Cesarean Section Scar Endometriosis: One Case and Literature Review 2025
- Ubiquitination of PFKFB4 by CHIP regulates glycolysis and progression in endometriosis† 2025
- PRMT3-mediated FOXO1 arginine methylation exacerbates oxidative stress-induced decidualization defects in the eutopic endometrium of endometriosis 2025
- Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3-Regulated HIF1A/HMOX1 Signaling Pathway 2025
- Ubiquitination of PFKFB4 by CHIP regulates glycolysis and progression in endometriosis† 2025
- Lactate-mediated immune suppression and MDSC expansion in endometriosis: Mechanisms and nanoparticle-targeted therapies 2025
- AURKA Enhances the Glycolysis and Development of Ovarian Endometriosis Through ERβ 2024
Source provenance
- europepmc
- last seen: 2026-06-18T06:15:08.409253+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-06-18T06:13:22.719913+00:00
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