Experimental Study Of TRA2B Promoting Proliferation,migration,invasion And Epithelial Mesenchymal Transformation Of Glioma Cells | | Posted on:2022-08-18 | Degree:Master | Type:Thesis | | Country:China | Candidate:H Y Shi | Full Text:PDF | | GTID:2504306722954439 | Subject:Surgery | | Abstract/Summary: | PDF Full Text Request | | Objective:To investigate the effects of transgenic gene TRA2 B on proliferation,migration,invasion and EMT of glioma cells.Methods:Glioma cell lines were transfected with lentivirus to knock down or overexpress TRA2 B.The expression of each gene was analyzed by real-time quantitative polymerase chain reaction,western blot,cell invasion assay,cell migration assay,cell proliferation assay and immunohistochemistry,and the protein was quantified by Quantity One software.SPSS26.0 was used for statistical analysis.Analysis of variance and t test were used for statistical difference analysis between groups.Results:The proliferation ability of U251 glioma cells was significantly reduced by TRA2 B knockdown.On the contrary,overexpression of TRA2 B significantly enhanced the proliferation of the cell line.Similarly,the invasion and migration ability of U251 glioma cells was significantly reduced when Tra2 B was knocked down,while the invasion and migration ability of U251 glioma cells was significantly enhanced when Tra2 B was overexpressed.Tra2 b knockdown in U251 glioma cells resulted in decreased expression of PCNA,MMP2,MMP9,Vimentin and N-cadherin,while increased expression of E-cadherin.The expression of PCNA,MMP2,MMP9,Vimentin and N-cadherin in U251 glioma was increased while the expression of E-cadherin was decreased when TRA2 B was overexpressed.Conclusion:TRA2B can promote proliferation,invasion,migration and epithelial mesenchymal transformation of glioma cells,suggesting that TRA2 B plays an important role in glioma progression,which may provide a new potential strategy for the treatment of glioma. | | Keywords/Search Tags: | TRA2B, glioma, proliferation, invasion, migration, EMT | PDF Full Text Request | Related items |
| |
|