Prostaglandin E(2) pathway in head and neck squamous cell carcinoma
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Updated: Jul 3, 2026

A Model for Perineural Invasion in Head and Neck Squamous Cell Carcinoma
Published on: January 5, 2017
Mercedes Camacho1, Xavier León, María-Teresa Fernández-Figueras
1Laboratory of Angiology, Vascular Biology and Inflammation, Institute of Research, Hospital Santa Creu i Sant Pau, Barcelona, Spain.
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.
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