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Prostaglandin E 2 pathway in head and neck squamous cell carcinoma
Author(s) -
Camacho Mercedes,
León Xavier,
FernándezFigueras MaríaTeresa,
Quer Miquel,
Vila Luis
Publication year - 2008
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.20850
Subject(s) - head and neck squamous cell carcinoma , prostaglandin e , prostaglandin , cyclooxygenase , prostaglandin e2 receptor , prostaglandin e2 , enzyme , cancer research , receptor , cell , head and neck , chemistry , cell growth , medicine , head and neck cancer , cancer , biochemistry , surgery , agonist
Background. Prostaglandin E 2 (PGE 2 ) is involved in malignant growth. The objective was to study the PGE 2 pathway in head and neck squamous cell carcinoma (HNSCC) patients. Methods. Expression of cyclooxygenase (COX) and PGE‐synthase isoenzymes, and PGE‐receptors was determined in biopsies from 83 patients with HNSCC by real‐time reverse transcriptase–polymerase chain reaction (RT‐PCR). Results. Expression of COX‐2 and cytosolic‐PGE‐synthase was significantly increased, about 4‐fold and 2.5‐fold, respectively, in tumors versus paired nontumoral mucosa ( n = 34). EP‐1 was the only PGE‐receptor significantly overexpressed in tumor samples. Expression of COX‐1 correlated with mPGES‐2 and COX‐2 correlated with mPGES‐1 ( n = 83). Conclusions. COX‐2, functionally coordinated with mPGES‐1, is likely to be the limiting enzyme in PGE 2 biosynthesis in HNSCC. The biological meaning of cPGES/p23 overexpression in HNSCC is not yet clear. Our results support the notion that mPGES‐1, cPGES, and EP‐1 could be the targets for the development of specific PGE 2 ‐modifier drugs for HNSCC treatment that could avoid negative side effects of COX‐2 selective inhibitors. © 2008 Wiley Periodicals, Inc. Head Neck 2008