Apigenin inhibits COX-2, PGE2, and EP1 and also initiates terminal differentiation in the epidermis of tumor bearing mice

Prostaglandins, Leukotrienes, and Essential Fatty Acids
Alex J KiralyRukiyah T Van Dross

Abstract

Non-melanoma skin cancer (NMSC) is the most prevalent cancer in the United States. NMSC overexpresses cyclooxygenase-2 (COX-2). COX-2 synthesizes prostaglandins such as PGE2 which promote proliferation and tumorigenesis by engaging G-protein-coupled prostaglandin E receptors (EP). Apigenin is a bioflavonoid that blocks mouse skin tumorigenesis induced by the chemical carcinogens, 7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA). However, the effect of apigenin on the COX-2 pathway has not been examined in the DMBA/TPA skin tumor model. In the present study, apigenin decreased tumor multiplicity and incidence in DMBA/TPA-treated SKH-1 mice. Analysis of the non-tumor epidermis revealed that apigenin reduced COX-2, PGE2, EP1, and EP2 synthesis and also increased terminal differentiation. In contrast, apigenin did not inhibit the COX-2 pathway or promote terminal differentiation in the tumors. Since fewer tumors developed in apigenin-treated animals which contained reduced epidermal COX-2 levels, our data suggest that apigenin may avert skin tumor development by blocking COX-2.

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Citations

Oct 25, 2016·Frontiers in Pharmacology·Daniel A LadinRukiyah Van Dross
Aug 31, 2016·The Journal of Pharmacology and Experimental Therapeutics·Samar Rezq, Abdel A Abdel-Rahman
Feb 6, 2018·Current Pharmacology Reports·Eswar ShankarSanjay Gupta
Oct 17, 2018·Future Medicinal Chemistry·Priyanka ChandelRupinder Kaur
Feb 15, 2020·Phytotherapy Research : PTR·Muhammad ImranJavad Sharifi-Rad
Oct 27, 2017·Frontiers in Pharmacology·Ken SoderstromRukiyah Van Dross
Dec 18, 2020·Life Sciences·Semim Akhtar AhmedAjaikumar B Kunnumakkara
Apr 14, 2021·Human & Experimental Toxicology·F Sahindokuyucu-KocasariS Garli
Jul 3, 2021·Cells·Álvaro Jara-Gutiérrez, Victoriano Baladrón

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