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Prostaglandins Leukot Essent Fatty Acids. 2016 Jan;104:44-53. doi: 10.1016/j.plefa.2015.11.006. Epub 2015 Dec 21.

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

Author information

1
Department of Pharmacology & Toxicology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
2
Department of Comparative Medicine, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
3
Department of Pharmacology & Toxicology, Brody School of Medicine, East Carolina University, Greenville, NC, USA. Electronic address: vandrossr@ecu.edu.

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.

KEYWORDS:

Apigenin; COX-2; Differentiation; EP1; Proliferation; Skin cancer

PMID:
26802941
DOI:
10.1016/j.plefa.2015.11.006
[Indexed for MEDLINE]

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