| Objective To investigate the effect of UNBS5162 on glioblastoma cell proliferation and metastasis in vitro, and to preliminarily explore its molecular mechanism. Methods Glioblastoma U251 cells were treated with 10 μmol/L UNBS5162 (as experimental group) or dimethyl sulfoxide (as control group), respectively. After treatment, the effect of UNBS5162 on cell proliferation, migration, invasion, and apoptosis of U251 cells were examined by CCK8 assay, Transwell assay and flow cytometry assay, respectively. The protein level of PI3K/AKT pathway-related proteins was examined by Western blot. Results The proliferation ability of UNBS5162 treated cells was significantly lower than that of control group (P<0.05). Compared with control group, the number of migrated cells and invaded cells all significantly decreased in UNBS5162 treated group. Moreover, the apoptotic rate of UNBS5162 treated group was significantly promoted compared with that of control group, and compared with control group, the expression level of anti-apoptotic protein Bcl-2 was down-regulated, while the expression levels of pro-apoptotic protein Bax and Active Caspase-3 were markedly up-regulated. Furthermore, compared with control group, the phosphorylation levels of the key proteins in PI3K/AKT pathway, AKT and mTOR, were all inhibited, and the downstream p70S6K protein expression also decreased. Conclusion UNBS5162 has significant inhibitory effect on cell proliferation and metastasis of glioblastoma cells by promoting apoptosis, and its mechanism might be related to the activity inhibition of PI3K/AKT signaling pathway in the glioblastoma cells. |
