›› 2011, Vol. 23 ›› Issue (2): 111-113.doi: 10.3969/j.issn.1004-616x.2011.02.007

• 论著 • Previous Articles     Next Articles

Effect of COX-2 gene antisense eukaryotic expression vector on SGC-7901 metastasis

MA Dan1, LIU Min2, WANG Ai-ping3, YANG Hua1,*   

  1. 1.Department of General Surgery, the Second Affiliated Hospital of the Third Military Medical University, Chongqing 400037; 2. Department of Neurosurgery, the Second Affiliated Hospital of the Third Military Medical University, Chongqing 400037; 3. Institute of Material Medica, Chinese Academy of Medical Sciences, Beijing 100050, China
  • Received:2010-07-13 Revised:2010-12-17 Online:2011-03-30 Published:2011-03-30
  • Contact: YANG Hua

Abstract: Use constructed antisense expression vector of human COX-2 gene and observe the relationship between COX-2 gene and tumor metastasis. METHODS: Gastric cancer cell line SCG-7901 was transfected with antisense expression vector of human COX-2 gene. Three groups of cells which included transfectant、SC236 treated group(SCG-7901 treated with COX-2 inhibitor SC236 at 100 μmol/L) and SCG-7901 as a control group. Changes of the invasion ability in each group were observed in vitro. Western blot was used to detect VEGF and MMP-2 expressions in the 3 groups. Then the transfectant and SCG-7901 were injected subcutaneously into BALB/C-nu/nu nude mice to develop transplantation tumor,another group of mice received SCG-7901 treated with SC236 injected subcutaneously. The sizes and the weights of the lesions were observed. RESULTS:The results of transwell membrane、 cell migration and the growth of transplanted tumors showed that after transfection the invasion ability of SCG-7901 was obviously inhibited, the expressions of VEGF and MMP-2 in the cell line decreased. CONCLUSION: Transfection with antisense expression vector of human COX-2 gene had obvious antitumor activity on metastasis of human gastric cancer cell line in nude mice. The mechanism may be via inhibition of angiogenesis and down-regulation of MMP-2 expression.

Key words: cyclooxygenase, antisense technology, recombinant vector, metastasis