Fig. 1: The in vitro antiproliferative activities of BKM120 and/or rucaparib in human GBM cells. | Cell Death & Disease

Fig. 1: The in vitro antiproliferative activities of BKM120 and/or rucaparib in human GBM cells.

From: BKM120 sensitizes glioblastoma to the PARP inhibitor rucaparib by suppressing homologous recombination repair

Fig. 1

A U251 and U87MG cells were treated with various concentrations of BKM120 and rucaparib (BKM-120 0.05, 0.1, 0.2, 0.5, 1, 2, 5, 10, 25 μM; rucaparib-0.2, 0.5, 1, 2, 5, 10, 25, 50, 100 μM), and antiproliferative effects were determined by MTT assay following 96 h incubation. B Cells were treated with BKM120 and rucaparib as single agents or in combination for 96 h and then subjected to MTT assay. The drug combination effects were analyzed using CalcuSyn software, and the resulting CI-Fa plots are shown. C U251 cells were treated with 0.5 μM BKM120 or/and 10 μM rucaparib, and U87 cells were treated with 1 μM BKM120 or/and 10 μM rucaparib (the same concentrations were used in subsequent experiments unless indicated) for 10 days and then stained with crystal violet. D Colonies with 50 or more cells were quantified using ImageJ. E Cells were treated with BKM120 and/or rucaparib for 24/48 h. After PI staining, flow cytometry analysis was performed to determine the cell cycle distribution. F Cell cycle distribution of the cells exposed to the single drugs or combination are represented as stacked columns. Statistical analysis of G2/M phase in each group. All data are presented as the mean ± SD (n = 3). *P < 0.05; **P < 0.01; ***P < 0.001.

Back to article page