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Correlation of Expression of Cyclooxygenase-2, Vascular Endothelial Growth Factor, and Peroxisome Proliferator–Activated Receptor  With Head and Neck Squamous Cell Carcinoma
Elise C. Jaeckel, MD;
Shefali Raja, BS;
Jian Tan, MD;
Sanjoy K. Das, PhD;
Sudhansu K. Dey, PhD;
Douglas A. Girod, MD;
Terrance T. Tsue, MD;
Thomas R. Sanford, MD
Arch Otolaryngol Head Neck Surg. 2001;127:1253-1259.
Cyclooxygenase (COX) is the rate-limiting enzyme in the formation of
prostaglandins from arachidonic acid. COX exists in 2 isoforms, COX-1 and
COX-2. These isoforms are encoded by separate genes and demonstrate cell-specific
expression and regulation. Peroxisome proliferator–activated receptor 
(PPAR) is a nuclear transcription factor that is activated by prostacyclin.
Vascular endothelial growth factor (VEGF) is a proangiogenic factor that is
up-regulated in various tumors. Vascular endothelial growth factor has been
shown to interact with COX-derived prostaglandins in angiogenesis. To better
understand the roles of these genes in head and neck squamous cell carcinoma
(HNSCCA), we examined the differential expression of the COX1, COX2, VEGF,
and PPAR genes in these tumors. Tissue samples
from patients with HNSCCA were analyzed for COX-1, COX-2, VEGF, and PPAR
messenger RNAs (mRNAs) by in situ hybridization. COX-1 and COX-2 mRNAs were
also evaluated with Northern blot hybridization. Immunohistochemistry was
used to analyze for COX-2 and PPAR proteins. Results showed focal areas
of accumulation for COX-2, VEGF, and PPAR but not COX-1 in human HNSCCA.
Northern blot hybridization showed higher levels of COX-2 mRNA in HNSCCA than
in normal tissue. This suggests a supportive role of COX-2 in development
and/or progression of HNSCCA. In addition, PPAR may be a receptor for
COX-2–produced prostaglandins in HNSCCA. There is a potential role for
selective COX-2 inhibitors in the treatment of these lesions.
From the Departments of Otolaryngology–Head and Neck Surgery
(Drs Jaeckel, Girod, Tsue, and Sanford) and Physiology (Ms Raja and Drs Tan,
Das, and Dey), University of Kansas Medical Center, Kansas City.
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