OBJECTIVE: To explore the role of ZNF217 in regulating cell proliferation, migration and invasion in glioma cells. METHDOS: A lentivirus-mediated shRNA-ZNF217 vector was infected into glioma U251 cells, and the interference efficiency was examined by Western blotting. MTT assay, flow cytometry, Transwell assay, and Boyden chamber assay were used to analyze the changes in cell proliferation, migration and invasion. Western blotting was used to detect the changes in ZNF217-related genes in the cells. RESULTS: shRNA-ZNF217 transfection significantly inhibited the expression of ZNF217 in U251 cells and suppressed the cell migration, invasion, growth, and cell cycle transition. ZNF217 knockdown downregulated the expression of pPI3, pAKT, C-Myc, and the mesenchyme biomarker N-cadherin, and stimulated the expression of the epithelium biomarker E-cadherin. CONCLUSION: ZNF217 promotes cell migration, invasion, and growth by activating PI3K/AKT signal to upregulate C-Myc and by modulating the genes associated with epithelial-mesenchymal transition in glioma cells.
OBJECTIVE: To explore the role of ZNF217 in regulating cell proliferation, migration and invasion in glioma cells. METHDOS: A lentivirus-mediated shRNA-ZNF217 vector was infected into glioma U251 cells, and the interference efficiency was examined by Western blotting. MTT assay, flow cytometry, Transwell assay, and Boyden chamber assay were used to analyze the changes in cell proliferation, migration and invasion. Western blotting was used to detect the changes in ZNF217-related genes in the cells. RESULTS: shRNA-ZNF217 transfection significantly inhibited the expression of ZNF217 in U251 cells and suppressed the cell migration, invasion, growth, and cell cycle transition. ZNF217 knockdown downregulated the expression of pPI3, pAKT, C-Myc, and the mesenchyme biomarker N-cadherin, and stimulated the expression of the epithelium biomarker E-cadherin. CONCLUSION: ZNF217 promotes cell migration, invasion, and growth by activating PI3K/AKT signal to upregulate C-Myc and by modulating the genes associated with epithelial-mesenchymal transition in glioma cells.