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Cyclooxygenase‐2: A Potential Target in the Treatment of Oral Cancers
Author(s) -
Masashi Hatori,
Nagumo Masao
Publication year - 2005
Publication title -
oral science international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.256
H-Index - 13
eISSN - 1881-4204
pISSN - 1348-8643
DOI - 10.1016/s1348-8643(05)80001-1
Subject(s) - carcinogenesis , cyclooxygenase , angiogenesis , cancer research , cancer , medicine , prostaglandin , prostaglandin e2 , cell growth , enzyme , pharmacology , immunology , biology , biochemistry
Results from epidemiological studies indicate that long‐term intake of non‐steroidal anti‐inflammatory drugs, which inhibit cyclooxygenase (COX) enzymes involved in prostaglandin biosynthesis, reduces the risk of several forms of human malignancies. Expression of COX‐2 in tumors is known to be associated with enhanced angiogenesis, suppression of host immunity, and tumor invasion. Genetic or pharmacological inhibition of COX‐2 has been shown to protect against experimentally‐induced carcinogenesis and to reduce the growth of xenografted tumors in animal models. A number of studies also revealed that COX‐2 inhibition suppresses proliferation, metastatic potential, and other functions of cancer cell lines. Thus, it is conceivable that targeted inhibition of abnormally or improperly elevated COX‐2 provides one of the most effective and promising strategies for cancer therapy. In this review, the involvement of COX‐2 in the tumorigenesis of oral cancers and the potential mechanisms of tumor suppressive effects of COX‐2 inhibition are discussed.