Fig. 7
AKT3-174aa negatively correlates the tumorigenicity of GBM cells in vivo. a U251, U373 cells with circ-AKT3 overexpression and their control cells were intracranially injected into nude mice (1X105 per mice, five mice per group). In vivo tumorigenicity was monitored, and mice were sacrificed when showing clinical symptoms. Mice brain were subjected to HE is staining or IHC staining as indicated. Survival analysis was calculated by Kaplan-Merier curve. *, p < 0.05. b SW1783, Hs683 cells with circ-AKT3 koncking down and their control cells were intracranially injected into nude mice (1X105 per mice, five mice per group). In vivo tumorigenicity was monitored, and mice were sacrificed when showing clinical symptoms. Mice brain were subjected to HE is staining or IHC staining as indicated. Survival analysis was calculated by Kaplan-Merier curve. *, p < 0.05. c Illustration of AKT3-174aa function. Normally, AKT3-174aa interacts p-PDK1 and limits AKT3 thr308 phosphorylation as a molecular decoy. In GBM, loss of AKT3-174aa exposed AKT thr308 to p-PDK1 more easily, promotes AKT activation and sequential signaling cascades