Abstract
Cyclooxygenase (COX) is a key enzyme responsible for developing several inflammatory diseases that may lead to cancer (Cox et al. 2004; Panguluri et al. 2004; Achyut et al. 2009; Park et al. 2006). Enhanced expression of COX-2 has been reported in many types of cancer, including esophageal and colorectal cancer (Upadhyay et al. 2009). Several studies suggest that COX-2-derived prostaglandins are mediators of carcinogenesis, influencing different hallmarks of cancer including hyperproliferation, transformation, tumor growth, invasion, angiogenesis, metastasis, and inhibition of apoptosis (Konturek et al. 2005; Greenhough et al. 2009; Pereira et al. 2006). The COX-2 enzyme may play a crucial role in the early stage of carcinogenesis (Wu et al. 2003; Liu et al. 2008). The promoter region of the COX-2 gene consists of multiple regulatory regions, suggesting a complex set of factors involved in its regulation (Xing et al. 2008). A functional promoter variant,
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