Epidemiological evidences suggest that chronic use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) might be associated with a reduced risk of gastrointestinal cancers, including gastric cancer. The pre-cancerous gastric lesions and gastric cancers over-expressed cyclooxygenase (COX)-2. This overexpression not only is associated with Helicobacter pylori infection, but also maybe due to exposure to carcinogens. Targeted inhibition of COX, especially the COX-2 isoform, can lead to growth inhibition and apoptosis of gastric cancer in vitro. Various mechanisms, including COX-dependent and COX-independent pathways, have been identified and will be discussed in this article. Animal xenograft models have confirmed the tumor suppressing effects of COX-2 inhibitors. Human studies are underway to examine the use of COX-2 inhibitor in the treatment of pre-cancerous lesions. COX-2 inhibitors have a promising role in the prevention and treatment of gastric cancer.
Keywords: gastric cancer, apoptosis, prostaglandin, cyclooxygenase, prevention, epidemiology, premalignant lesions, intervention
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