ecdysterone and Glioblastoma

In this study, gene transfection was used to determine whether the exogenous expression of p16INK4a modulated the biological characteristics of glioblastoma cells. The human glioblastoma cell line U87MG was doubly transfected with the plasmids pVgRXR and pIND harboring the wild-type p16 gene. The expression of p16INK4a in the resulting transfectants was regulated by the addition of the ecdysone homologue, muristerone A. When the cells expressed p16INK4a, their growth capacity was reduced and morphological changes such as an increase in cell size and cellular flattening were observed. The analysis of cell cycle regulation provided evidence that cells expressing p16INK4a were inhibited from entry into the cell cycle, as assessed by Ki-67 antigen expression. In addition, it was observed that the exogenous expression of p16INK4a was associated with decrease in telomerase activity.

Topics: Brain Neoplasms; Cell Cycle; Cell Division; Clone Cells; Cyclin-Dependent Kinase Inhibitor p16; Ecdysterone; Gene Expression Regulation; Glioblastoma; Humans; Microscopy, Electron, Scanning; Plasmids; Recombinant Proteins; Telomerase; Transfection; Tumor Cells, Cultured