| Background: Gastric cancer is a common digestive tract tumor among Chinese residents,and its morbidity and mortality have been at a high level.Many literatures have confirmed that the high expression of prrx1 can promote gastric cancer cells to start EMT program,and the activation of EMT program can promote the formation of vasculogenic mimicry.Objective: The purpose of this study was to explore the relationship between the invasion and migration of prrx1 gene and the number of VM production in gastric cancer cells.Methods: MNK45 gastric cancer cell line and SGC7901 gastric cancer cell line with high and low expression of prrx1 gene were established in vitro.The cells were divided into MNK45 group,MNK45 overexpression group(MNK45(O)),SGC7901 group,SGC7901 inhibition group(SGC7901i))and blank control cell models of MNK45(NC)and SGC7901 NC.The transfection effect of each cell line was evaluated by Western blot detection of PRRX1 and its related protein content.Scratch test and Transwell assay were used to detect the effect of gene transfection on the migration and invasion of gastric cancer cells.Cell 3D culture was used to observe the number of angiogenic mimicry channels formed by cells.Results:1.The transfected gastric cancer cell line was adherent to the wall in the cell culture flask and showed green under fluorescence.2.After transfection,the expression of PRRX1 and Vimentin protein in overexpression group was higher than that in blank control group and untreated group,while the content of E-cadherin protein in overexpressed group was lower than that in blank control group and untreated group.After transfection,the expression of PRRX1 and Vimentin protein in the inhibition group was lower than that in the blank control group and untreated group,and the content of E-cadherin protein in the inhibition group was significantly higher than that in the blank control group and untreated group(P<0.01).3.The results of scratch experiment: the healing area of overexpression group was larger than that of blank control group and untreated group after transfection,and the difference was statistically significant(P<0.01).After transfection,the healing area of the inhibition group was smaller than that of the blank control group and the untreated group,and the difference was statistically significant(P<0.01).The results of 4.Transwell assay showed that the number of transmembrane cells in the overexpression group was higher than that in the blank control group and the untreated group,and the difference was statistically significant(P<0.01).After transfection,the number of transmembrane cells in the inhibition group was less than that in the blank control group and the untreated group,and the difference was statistically significant(P < 0.01).5.3D culture results: after transfection,the number of VM ducts in theover-expressed group was larger than that in the blank control group and untreated group,and the difference was statistically significant(P<0.01).After transfection,the number of VM ducts in the inhibition group was less than that in the blank control group and the untreated group,and the difference was statistically significant(P<0.01).Conclusion:The expression of 1.prrx1 can enhance the invasion and migration of gastric cancer cells,and the expression of 2.prrx1 can increase the number of VM channels formed by gastric cancer cells. |
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