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Cetrorelix promotes cell apoptosis via the PI3K-AKT-FOXO1 pathway in epithelial ovarian cancer.

Ning Zhang1,2, Yu Liu1,2, Xiaodan Zhang1,2

  • 1Department of Gynecology, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China.

Frontiers in Oncology
|December 29, 2025
PubMed
Summary

Cetrorelix induces epithelial ovarian cancer (EOC) apoptosis through the PI3K/AKT-FOXO1 pathway, offering potential for GnRH antagonists in EOC treatment. Clinical markers like GnRHR and AKT expression correlate with improved patient survival.

Keywords:
PI3K–AKT–FOXO1 pathwayapoptosiscetrorelixepithelial ovarian cancergonadotropin-releasing hormone antagonist

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Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Epithelial ovarian cancer (EOC) has a poor prognosis with limited therapeutic options.
  • Understanding novel therapeutic mechanisms is crucial for improving EOC patient outcomes.

Purpose of the Study:

  • To elucidate the mechanism of cetrorelix in inducing EOC apoptosis.
  • To evaluate the clinical significance of Gonadotropin-releasing hormone receptor (GnRHR), AKT, and Forkhead box protein O1 (FOXO1) in EOC patients.

Main Methods:

  • In vitro and in vivo models were used to assess cetrorelix-induced apoptosis via flow cytometry, Hoechst staining, and Western blotting.
  • Gene knockdown studies (siRNA) and pathway inhibitors (LY294002) explored the PI3K/AKT/FOXO1 signaling axis.
  • Immunohistochemistry and survival analyses (Kaplan-Meier, Cox regression) were performed on EOC patient tissues.

Main Results:

  • Cetrorelix promoted EOC apoptosis by upregulating FOXO1 and downregulating p-AKT through the PI3K/AKT pathway.
  • GnRHR knockdown abrogated cetrorelix-induced apoptosis, confirming receptor specificity.
  • FOXO1/GnRHR positivity and AKT negativity correlated with early-stage disease and improved survival in EOC patients.

Conclusions:

  • Cetrorelix induces EOC apoptosis via the PI3K/AKT-FOXO1 pathway, supporting GnRH antagonists as a therapeutic strategy for EOC.
  • GnRHR, AKT, and FOXO1 represent potential therapeutic targets for managing epithelial ovarian cancer.