OBJECTIVETo explore the role of ZNF217 in regulating cell proliferation, migration and invasion in glioma cells.

METHDOSA 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.

RESULTSshRNA-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.

CONCLUSIONZNF217 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.

Cadherins ; metabolism ; Cell Cycle ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Epithelial-Mesenchymal Transition ; Genetic Vectors ; Glioma ; pathology ; Humans ; Lentivirus ; Neoplasm Invasiveness ; RNA, Messenger ; RNA, Small Interfering ; genetics ; Trans-Activators ; genetics ; Transfection

OBJECTIVE: To investigate the effect of curcumin on the invasion and migration of human glioma cells and explore the molecular mechanisms. METHODS: MTT assay was used for screening the optimal curcumin concentrations. The effects of curcumin on the invasion and metastasis of human glioma cell lines U251 and LN229 were tested using Transwell assay, Boyden assay and wound-healing assays. The expression of the related proteins and their interactions were determined using Western blotting and coimmunoprecipitation assay. RESULTS: Curcumin at the concentration of 20 μmol/L for 48 h was used as the optimal condition for subsequent cell treatment. In the two glioma cell lines, curcumin significantly suppressed the invasion and migration of the cells ( < 0.05) and lowered the expressions of hepatoma-derived growth factor (HDGF), Ncadherin, vimentin, Snail and Slug, but increased the expression of E-cadherin. Interference of HDGF in curcumin-treated glioma cells synergistically inhibited the epithelial-mesenchymal transition (EMT) signals, while overexpression of HDGF significantly reversed the inhibitory effect of curcumin on EMT; curcumin treatment could significantly reduce the binding of HDGF to β-catenin. CONCLUSIONS Curcumin suppresses EMT signal by reducing HDGF/β-catenin complex and thereby lowers the migration and invasion abilities of human glioma cells .
Cell Line, Tumor ; Cell Movement ; Curcumin ; Epithelial-Mesenchymal Transition ; Glioma ; Humans ; Intercellular Signaling Peptides and Proteins ; Neoplasm Invasiveness ; beta Catenin