Expression of PGDH correlates with cell growth in both esophageal squamous cell carcinoma and adenocarcinoma.

Guo-Tao Yang,Xue-Fei Sun,Juan Wang,Zi-Ying Luan,Tong-Zhen Xu

doi:10.7314/apjcp.2015.16.3.997

Abstract

Esophageal cancer represents the fourth most common gastrointestinal cancer and generally confers a poor prognosis. Prostaglandin-producing cyclo-oxygenase has been implicated in the pathogenesis of esophageal cancer growth. Here we report that prostaglandin dehydrogenase, the major enzyme responsible for prostaglandin degradation, is significantly reduced in expression in esophageal cancer in comparison to normal esophageal tissue. Reconstitution of PGDH expression in esophageal cancer cells suppresses cancer cell growth, at least in part through preventing cell proliferation and promoting cell apoptosis. The tumor suppressive role of PGDH applies equally to both squamous cell carcinoma and adenocarcinoma, which enriches our understanding of the pathogenesis of esophageal cancer and may provide an important therapeutic target.

Highlights

Esophageal cancers represent the fourth most common gastrointestinal cancer and rank among the ten most common cancers worldwide (Siegel et al, 2011; Dabrowski et al, 2012; Silva et al, 2012)
Cox-2 specific inhibitors have been developed to target on malignant tissue growth and have achieved clinical benefit, the cardiovascular side-effects associated with their use have greatly hampered their popularity (Doll et al, 2012; Ho et al, 2012; Katkoori et al, 2012)
We examined the Prostaglandin hydrogenase (PGDH) expression at RNA and protein level in esophageal cancer and normal esophageal epithelium

Summary

Introduction

Esophageal cancers represent the fourth most common gastrointestinal cancer and rank among the ten most common cancers worldwide (Siegel et al, 2011; Dabrowski et al, 2012; Silva et al, 2012). Cyclooxygenase-2 (COX-2), the enzyme leading to prostaglandin synthesis, is over-expressed in esophageal cancer and other gastrointestinal cancers and generally not expressed in normal epithelium (Shan et al, 2012; Wang et al, 2012; Zhang et al, 2012; Castro-Sanchez et al, 2013; Lee et al, 2013). Cox-2 specific inhibitors have been developed to target on malignant tissue growth and have achieved clinical benefit, the cardiovascular side-effects associated with their use have greatly hampered their popularity (Doll et al, 2012; Ho et al, 2012; Katkoori et al, 2012). The definitive chemopreventive benefit derived from use of Cox-2 specific inhibitors confirms that prostaglandin pathway can serve as a valid target for chemoprevention

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