| Background and Objective Gastric cancer is a common neoplasm with highest mortality in all the malignant neoplasms for a long time. With more attention to early discovery and diagnosis, there is an obvious decrease of its mortality, yet we still have lots of trouble in treating it, especially when facing advanced gastric cancer. Finding new and effective methods to decrease its incidence and mortality is badly needed. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, indomethacin and sulindac, showed by lots of evidence, have the effect of suppressing tumor proliferation and inducing apoptosis besides its effect of anti-inflammation, relieving pain, and anti-coagulation of platelets. Long-time aspirin used can obviously decrease the mortality of colonic adenocarcinoma. Sulindac was also found to be effective in treating familial adenomatous polyposis (FAP) and can reduce the mortality of colonic adenocarcinoma. Studies showed that the anti-tumor effect of NSAIDs was partly mediated through its inhibition of the COX-2 activity. COX is a key enzyme in prostaglandin biosynthesis. Two isoforms of COX have been identified: constitutively expressed COX-1 and mitogen-inducible COX-2. Recent studies have demonstrated that COX-2 could affect carcinogenesis via several different mechanisms. One of the important mechanisms of COX-2 involving in carcinoma is that COX-2 enhances tumor angiogenesis, which might be essential for tumor growth. Prostaglandin product of arachidonic acid metabolism catalyzed by COX-2 may be angiogenesis promoter of carcinoma. Vascular endothelial growth factor (VEGF), is the mostpowerful factor involving in the process of angiogenesis. Evidences showed that COX-2 can up-regulate the expression of VEGF in tumor tissues while inhibiting COX-2 activity can down-regulate the expression of VEGF. Our experiments try to observe the effects of aspirin on gastric cancer cell line SGC7901, and to explore the underlining mechanism. Methods SGC7901 cells were treated with aspirin (0.1mmol/L, 1.0mmol/L, 8.0mmol/L) for 24 h, the expression of COX-2 and VEGF protein of SGC7901 cells was evaluated by immunocytochemical method and Western blot; the cell cycle were analyzed by flow cytometry (FCM); MTT reduction assay was used to evaluate the inhibitory rate of SGC7901 cells treated with aspirin for 24 h, 48 h and 72 h.Results (1) The inhibitory rate of aspirin on SGC7901 cell proliferation increased as incubation time (F=402.062 .P=0.000) and aspirin concentration (F=50.141 P=0.000) increasing. ( 2) The percentage of G0IG1 phase in control group was 56.4%; 61.9% in O.lmmol/L aspirin treated group; 64.6% in l.Ommol/L aspirin treated group; and 67.2% in 8.0mmol/L aspirin treated group, aspirin increased the proportion of cells in the G0/G1 phase of the cell cycle. (3) When the concentrations of aspirin were 0mmol/L,0.1mmol/L,1.0 mmol/L,8.Gmmol/L, the A values of COX-2 protein expression were 0.675 + 0.031,0.660 + 0.023,0.597 + 0.016,0.578 + 0.014. Compared with the group that aspirin concentration was 0mmol/L, the groups that aspirin concentrations were 1.0mmol/L and 8.0mmol/L could significantly inhibit the COX-2 protein expression level (P< 0.05); the A values of VEGF protein expression were 0.480+0.014 0.457+0.027 0.407+0.032. 0.363 + 0.029 when the concentrations of aspirin were 0mmol/L,0.1mmol/L,1.0 mmol/L,8.0mmol/L. Compared with the group that aspirin concentration was 0mmol/L, the groups that aspirin concentrations were 1.0mmol/L and 8.0mmol/L could significantly inhibit the VEGF protein expression level (P<0.05) (4) When the concentrations of aspirin were 0mmol/L,0.1mmol/L,1.0 mmol/L,8.0mmol/L, the density values of COX-2 bands were 120,105, 86,65, aspirin could decrease the protein level of COX-2; The density values of VEGF bands were 125, 118, 98 and 76 when the concentrations of aspirin were 0mmol/L,0.1mmol/L,1.0 mmol/L,8.0mmol/L,aspirin could decrease the protein level of VEGF.Conclusion Aspirin has inhibitory effect on SGC7901 cel...
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