| Objective:See NCOA2 genes in MKN-28 and BGC-823 gastric cancer cell proliferation,metastasis and invasion effect,and to explore its possible mechanisms.Methods:1.Using immunohistochemical staining method,comparison between NCOA2 gene and the clinical pathological features of gastric cancer and the expression differences between cancerous tissues and normal tissues,to prepare for the further research of this study provide new clues and mechanism research.2.To slow virus interference NCOA2 gene expression,using Western Blotting detection and Wnt pathways and EMT related protein expression3.Application tablet cloning experiments,CCK 8 experiments and Transwell of different cells’ functions experiment,to explore the expression of interference NCOA2 after gastric cancer cell proliferation,metastasis and invasion ability of change.4.Comparison of inhibition of NCOA2 expression before and after gastric cancer cell apoptosis ability difference.5.Inhibition of NCOA2 gene expression before and after the stable gastric cancer cells were injected into the mouse subcutaneous and intraperitoneal,compared with in vivo on gastric cancer subcutaneous and peritoneal metastasis differences.Results:1.The immunohistochemistry results showed that: the gastric cancer and adjacent tissue by immunohistochemical staining,we found that not only the expression of NCOA2 with lymph node metastasis,TNM staging and gender differences,and the difference was statistically significant(P<0.05),but not with other clinicopathologic factors including age,tumor size,distant metastasis.2.The results of Western blotting showed that the expression of β-catenin was decreased after the expression of NCOA2,but E-cadherin decreased.Following the reduction of E-cadherin,N-cadherin,Vimentin and Slug were significantly increased..3.Colony formation and CCK-8 experimental results show that after the expression of NCOA2 was inhibited,the number of gastric cancer cells was significantly decreased,and the CCK-8 experiment measured the OD values significantly different,and the difference was statistically significant(P<0.05).4.Transwell experiment: the number of the cells through the small room of the membrane after NCOA2 is disturbed is less than normal express NCOA2 gastric cancer cells.Then we count the number of passes through the cell membrane of the cell,and the experimental group and the control group were examined by T test.The comparison results showed that the difference was statistically significant(P < 0.05).5.Apoptosis: After interfering with the expression of NCOA2,the number of cells in early and late stage of gastric cancer cells was significantly increased.6.Animal experiments: after interfering with the expression of NCOA2,the number of MKN-28 sh cells implanted in the abdominal cavity of nude mice was less than that of MKN-28 nc cells,and the size was smaller.The experimental group and the control group in nude mice in the abdominal cavity of the number of T test,the results showed that the difference was statistically significant(P < 0.05).The size of MKN-28 sh cells in the experimental group was smaller than that in the control group Conclusion:1.The positive rate of NCOA2 in patients with gastric cancer is high,and its expression is not only related to lymph node metastasis,TNM stage,but also related to sex;2 The expression of NCOA2 gene can activate the Wnt pathway,promote the epithelial mesenchymal transition(EMT)of gastric cancer cells,and promote the proliferation and metastasis of tumor cells;3.Both in vitro and in vivo,NCOA2 can not only promote the proliferation and survival of human gastric cancer cell line MKN-28 and BGC-823,but also through the inhibition of apoptosis,promote its metastasis and invasion,and enhance cell viability. |
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