Skip to main content
. 2022 Apr 14;12(4):580. doi: 10.3390/life12040580

Figure 4.

Figure 4

Effects of the AKT inhibitor capivasertib on cell proliferation and apoptosis. (A) Low-passage glioblastoma cells (HROG02, HROG05, HROG15, HROG17, and HROG24) and brain metastasis cells (HROBMC01 and HROBML01) growing in 96-well half-area microplates were treated with capivasertib (striated bars) or solvent (black bars) for 48 h, before DNA synthesis was assessed with the BrdU incorporation assay. One hundred percent BrdU incorporation corresponds to cells cultured with solvent only. Data are presented as mean ± SEM (n ≥ 18 separate cultures); * p < 0.05 versus control cultures (Kruskal–Wallis test with post hoc Dunn’s test). (B) Subconfluent-growing glioblastoma cells were challenged with capivasertib (striated bars) or solvent (black bars) for 6 h followed by caspase 3/7 enzyme activity quantification. Data are presented as mean ± SEM (n ≥ 9 separate cultures for caspase activity assay); * p < 0.05 versus control cultures (Kruskal–Wallis test with post hoc Dunn’s test).