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COX-2-PGE2-EPs in gynecological cancers

Ye Yao, Xipeng Wang, Udo Jeschke, Viktoria von Schönfeldt

2020Archives of Gynecology and Obstetrics82 citationsDOIOpen Access PDF

Abstract

Abstract Purpose Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors (COXibs) inhibit the progression of endometrial cancer, ovarian cancer and cervical cancer. However, concerning the adverse effects of NSAIDs and COXibs, it is still urgent and necessary to explore novel and specific anti-inflammation targets for potential chemoprevention. The signaling of cyclooxygenase 2-prostaglandin E 2 -prostaglandin E 2 receptors (COX-2-PGE 2 -EPs) is the central inflammatory pathway involved in the gynecological carcinogenesis. Methods Literature searches were performed to the function of COX-2-PGE 2 -EPs in gynecological malignancies. Results This review provides an overview of the current knowledge of COX-2-PGE 2 -EPs signaling in endometrial cancer, ovarian cancer and cervical cancer. Many studies demonstrated the upregulated expression of the whole signaling pathway in gynecological malignancies and some focused on the function of COX-2 and cAMP-linked EP2/EP4 and EP3 signaling pathway in gynecological cancer. By contrast, roles of EP1 and the exact pathological mechanisms have not been completely clarified. The studies concerning EP receptors in gynecological cancers highlight the potential advantage of combining COX enzyme inhibitors with EP receptor antagonists as therapeutic agents in gynecological cancers. Conclusion EPs represent promising anti-inflammation biomarkers for gynecological cancer and may be novel treatment targets in the near future.

Topics & Concepts

MedicineEndometrial cancerCervical cancerOvarian cancerProstaglandin E2 receptorCancerCyclooxygenaseCarcinogenesisInflammationProstaglandin E2Prostaglandin EReceptorProstaglandinInternal medicineOncologyCancer researchEnzymeBiologyBiochemistryAgonistInflammatory mediators and NSAID effectsCancer, Stress, Anesthesia, and Immune ResponseEstrogen and related hormone effects
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