BACKGROUND: Glioma is one of the most common primary malignant brain tumors. However, the potential molecular mechanism of glioma tumorigenesis is limited. In this study, we aimed to investigate the functional relationship between glioma and a potential tumor related geneJUB.
METHODS: Lentivirus-based RNA interference was carried out to knock down JUB expression in human glioma cells U251. The effects ofJUB on cell proliferation and cell cycle were detected by MTT, colony formation and flow cytometry assays.
RESULTS: Lentivirus-mediated shRNA could effectively suppress JUB expression in U251 cells, resulting in significant decreases in cell proliferation and colony formation. Flow cytometry analysis showed thatJUB silencing blocked cell cycle at S and G2/M phases, and induced apoptosis, which could contribute to cell growth suppression. Furthermore, knockdown ofJUB caused downregulation of CDK6 and activations of Caspase 3 and PARP.
CONCLUSIONS: The results in this study uncovered that JUB was a regulator involved in proliferation of glioma cells, and it could be used as a potential therapeutic target for glioma.
