| Objective: HCC is the leading cause of malignant cancer death in the world . However, the exact molecular mechanism of hepatocarcinogenesis is still unclear. Unfortunately, to date, there is no effective preventive measure for this highly malignant disease.Empirically, inhibition of COX-2 with NSAIDs such as aspirin could induce the regression of colon polyps in patients with familial adenomatous polyposis. The incidence rate of colon carcinoma can be cut down 40%-50% by using NSAIDs. Furthermore, a selective inhibition of COX-2 brought the nearly complete suppression of azoxymethane-induced colon cancer. COX-2 has also been found to be high in other types of cancers including prostate, breast, gastric, pancreatic, lung, and head and neck cancers. COX, known as PG synthase, catalyzes the metabolism of arachidonic acid to PGs and thromboxanes , and two isoforms, COX-1 and COX-2, have been identified. COX-1 is constitutively present in many cell types and is responsible for various cytoprotective prostanoids in a number of organs, such as the gastric mucosa and the kidneys, whereas COX-2 is usually absent under basal conditions but inducible in certain cells by mitogens, cytokines, and other factors. COX-2 has recently been categorized as an immediate-early gene associated with inflammation, cellular growth, differentiation, prevention of apoptosis, and tumorigenesis. It has also been reported that COX-2 induces angiogenesis, which is essential for tumor growth. Increased prostaglandin production and enhanced release of angiogenic growth factor by COX-2 may induce neovascularization.In HCC, It was reported that abnormal COX-2 expression plays an important role in hepatocarcinogenesis. In the present study, the expression...
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