动物造模,血管生成素-2 z-bio 2021-02-21 296

　　Objective: To investigate the relationship between O-N-acetylglucosamine (O-GlcNAc) glycosylation level and the expression of Angiopoietin-2 (Ang-2) in the process of liver cancer.

　　 Method: Use diethyl nitramine (DEN) to induce C57BL/6 mouse liver cancer model, and detect O-GlcNAc glycosylation, Ang-2 and endothelial cell adhesion molecule (CD31) expression in liver cancer. -Acetyl Glucosamine Transferase (OGT) inhibitor N-Acetyl Glucosaminidase (OGA) inhibitor interferes with HepG2 cells and detects whether Ang-2 expression changes with changes in O-GlcNAc glycosylation level. MTT is used to detect O-. The relationship between GlcNAc glycosylation level and the proliferation of liver cancer cells; Transwell method was used to detect the relationship between O-GleNAc glycosylation level and HUVEC cell migration and infiltration capacity.

　　Result: In the DEN-induced liver cancer model, the liver of mice increased significantly, and tumors of various sizes were found in the liver. Immunohistochemistry results showed that the O-GlcNAc glycosylation level and Ang-2 expression level in the liver of the model group were significantly higher than those of the control group and CD31 stained microvessels (P\u003c0.05), and the liver density was significantly increased. Cancer tissue (P\u003c0.01); qRT-PCR test results showed that by detecting the levels of OGT, OG4 and Ang-2 mRNA, the glycosylation level of O-GleNAc is Ang. It affects the level of expression. -2; Westembloting results showed that after drug intervention in HepG2 cells, the use of OGT inhibition can reduce the expression of Ang-2 and at the same time reduce the level of O-GlcNAc glycosylation; after drug intervention on the inhibitory effect of OGA on HepG2 cells, Ang expression 2 As O increases, it increases and increases the level of -GlcNAc glycosylation. MTT results indicate that the glycosylation level of O-GleNAc is closely related to the proliferation of liver cancer cells. The high level of O-GlcNAc glycosylation increases the proliferation ability of liver cancer cells. When the glycosylation level of O-GlcNAc is low, the proliferation ability of liver cancer cells is obviously inhibited. Transwell results showed that the migration and infiltration capacity of HUVEC cells was positively correlated with the glycosylation level of O-GleNAc.

　　 Conclusion: During the occurrence and development of liver cancer, the level of O-GlcNAc glycosylation gradually increases, and the expression level of Ang-2 is positively regulated by O-GlcNAc glycosylation, thereby promoting tumor angiogenesis.