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Carcinogenesis Advance Access published online on December 13, 2005
Carcinogenesis, doi:10.1093/carcin/bgi304
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received August 5, 2005
Revised August 30, 2005
Accepted December 6, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Significance of COX-2 expression in human esophageal squamous cell carcinoma

Huiying Zhi 1, Lin Wang 1, Jian Zhang 1, Chunnong Zhou 1, Fang Ding 1, Aiping Luo 1, Min Wu 1, Qimin Zhan 1, and Zhihua Liu 1 *

1 National Laboratory of Molecular Oncology, Cancer Institute, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100021, P. R. China

* To whom correspondence should be addressed.
Zhihua Liu, E-mail: liuzh{at}pubem.cicams.ac.cn


  Abstract

Cyclooxygenase-2 (COX-2) is well established to play an important role in the tumorigenesis of a variety of human cancers; however, the function of COX-2 in the development of esophageal squamous cell carcinoma (ESCC) remains less clear. Here, we determined, first, the pattern of COX-2 expression in normal esophageal mucosa, dysplasia, carcinoma in situ (CIS), and invasive SCC. Immunohistochemical analysis showed that, while COX-2 was weakly expressed, if at all, in normal squamous epithelium, strong COX-2 expression was detected as early as the stage of dysplasia and frequently in 20 of 26 (77%) in situ carcinoma and 86 of 111 (77%) invasive SCC. Up-regulation of COX-2 in ESCC was found to be significantly associated with tumor progression (R=0.493,P<0.01). Further, treatment of human ESCC cell lines (KYSE450 and KYSE510) with NS-398, a COX-2 specific chemical inhibitor, suppressed the production of prostaglandin E2 (PGE2) and induced cell growth inhibition, cell cycle arrest at the G1-S checkpoint, and the expression of cyclin-dependent kinase inhibitors p21waf1/cip1 and p27kip1. Finally, knock-down expression of COX-2 in KYSE450 cells by a specific COX-2 siRNA dramatically inhibited PGE2 production, cell growth, and, more importantly, colony formation and tumorigenesis in nude mice. Together, this study suggested that COX-2 may be involved in an early stage of squamous cell carcinogenesis of the esophagus and has a non-redundant role in the regulation of cellular proliferation and tumorigenesis of esophageal epithelial cells.


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