Baicalein inhibits invasion and promotes apoptosis in glioma cells through the PI3K/Akt pathway.

PURPOSE

The purpose of this study was to elucidate the role of Baicalein in accelerating invasiveness and inducing apoptosis of glioma cells through the phosphatidilinositol 3-kinase/protein kinase B (PI3K/Akt) pathway.

METHODS

U251 glioma cells were treated with different doses of Baicalein (10, 20 or 40 μM) for different time periods (12, 24, 36 or 48 h). Changes in viability, clonality, cell cycle distribution and apoptosis in Baicalein-treated U251 cells were assessed. Meanwhile, relative levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 in U251 cells were detected. Western blot was conducted to examine protein levels of p-Akt and Akt in Baicalein-treated U251 cells.

RESULTS

Baicalein treatment attenuated dose-dependently and time-dependently the viability and clonality in U251 cells. It induced cell cycle arrest in G0/G1 phase and cell apoptosis of U251 cells. After Baicalein treatment, the relative levels of MMP-2 and MMP-9 were dose-dependently downregulated. Baicalein treatment activated the PI3K/Akt pathway. Notably, inhibitory effects of Baicalein treatment on MMP levels and invasiveness in glioma were blocked by the application of LY294002 (PI3K/Akt inhibitor), and stimulated by the application of IGF-1 (PI3K/Akt activator).

CONCLUSIONS

Baicalein treatment is able to suppress invasiveness and induce apoptosis of glioma cells through inactivating the PI3K/Akt pathway.