| Polyunsaturated fatty acids which are vital component of cell membranes cannot be synthesized by the body and must be obtained from food. These essential fatty acids are specific precursors of the eicosanoids, which regulate numerous cell and organ functions. Omega-3 polyunsaturated fatty acids (n-3PUFAs), which serve as essential nutrients in normal retina and brain development, play an important role in prevention and treatment of chronic cardiovascular disease, and arthritic disorders, and diabetes mellitus. Both of epidemiologic and experimental study support that the long-chain n-3PUFAs, which occur at high levels in some marine fish oils and soybean oils, exert protective effects against some common cancers, especially those of breast, colon, prostate, and perhaps pancreas. In the contrast, n-6PUFAs mainly obtained from corn oils may involved in carcinogenesis of some cancers, which is correlated with the arachnidonic acid-derived eicosanoids, such as prostaglandin E2, and thromboxane A2, and hydroxyleicosatetraenic acids(HETEs), and leukotrienes(LTs).The n-3PUFAs are represented by a-Linolenic acid (LNA) and n-6PUFAs by linoleic acid (LA). Both LNA and LA are metabolized to longer-chain fatty acids, mainly in the liver. LNA is converted to Eicosapentaenoic acid(EPA), and then to Docosahexaenoic acid(DHA), while LA is metalolic precursor of arachidonic acid(AA). Both n-3PUFAs and n-6PUFAs may be elongate and desaturated to longer-chain fatty acids of the same series, but they cannot be interconverted. n-3PUFAs have greater affinities for elongases and desaturases, so the production of AA, which may contributeto cell proliferation and inflammation, will be inhibited by increasing the dietary intake of n-3PUFAs.Recent studies have demonstrated that many mechanisms are involved in the inhibitory effects of n-3PUFAs on growth and metastasis of cancers, including COX-2 inhibition, lipoxygenase inhibition, enhancing lipid peroxidation, antiangiogenesity, arrest cell cycle, modify immune responses, influencing the expression of genes which are associated with cell proliferation, influencing the expression of protein kinase and protein phosphatase.COX-2 overexpression occurs in a variety of human cancers and there is both epidemiologic and experimental evidence to suggest that COX-2 may play some role in some cancers initiation and progression. COX-2 is a key regulating enzyme hi the synthesis of PGE2 which promotes cell proliferation and angiogenesis, makes cells resistant to apoptosis, enhances invasiveness, and modulates immunosuppression. Many experimental and clinical studies indicate that COX-2 inhibitors have a significantly suppressive effect on tumor growth, angiogenesis, and metastasis in many common cancers, such as breast, colon, and stomach. n-3PUFAs can inhibit the expression of COX-2 and effectively compete with AA for COX-2 activity and reduce production of AA-derived eicosanoids, which tend to promote inflammation and cell proliferation. To investigate whether n-3PUFAs have same suppressive effect on gastric cancer, we utilized the AGS cell line to demonstrate it in vitro. 1. DHA inhibit cell proliferation in AGS cell lineDHA with 22-carbons and 6 double bonds is the extreme example of n-3PUFAs. Recent studies suggest DHA can suppress cell proliferation and induce cell apoptosis in various tumor cells. The human gastric cancer cell line AGS was seeded into 96-well microplates, and cultured in 200ul RPMI1640 medium supplemented with DHA, at concentration ranging from 10ug/ml to 100ug/ml. After incubation for 24h, cell viability and proliferation was determined by MTT colourimetric assay. The cell viability of thenormal intestinal epithelium incubated with DHA was also measured. The results of the MTT assay demonstrated that DHA effectively inhibit AGS cell proliferation with dose-dependent and time-dependent, but not affected growth of the normal intestinal epithelium even at concentration of 100ug/ml.2. DHA induce apoptosis in AGS cell lineTo investigate whether apopt...
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