Fig. 6

The ATM-PKM2-CtIP axis provides resistance to genotoxic agents. a U87 shCtrl and shPKM2 cells, and shPKM2 cells expressing shRNA-resistant WT or T328A PKM2, were irradiated with 6 Gy. The number of viable cells was determined by trypan blue staining at the indicated time points. Data are the relative mean fraction of surviving cells ± SE (n = 3). b WT or T328E PKM2 was overexpressed in U87 cells. Cells were pre-treated with DMSO or 10 µM KU55933 and then irradiated. The number of viable cells was determined by trypan blue staining at the indicated time points. Data are the relative mean fraction of surviving cells ± SE (n = 3). c U87 shCtrl or shPKM2 cells, and shPKM2 cells overexpressing WT or T126E CtIP, were irradiated and the number of viable cells was determined by trypan blue staining at the indicated time points. Data are the relative mean fraction of surviving cells ± SE (n = 3). d U87 shCtrl or shPKM2 cells, and shPKM2 cells expressing shRNA-resistant WT, T328A, or T328E PKM2 were incubated with the indicated concentrations of olaparib. Cell viability was determined by trypan blue staining 48 h after treatment. Data are the relative mean fraction of surviving cells ± SE (n = 3). e Representative 10 × and 40 × images from GBM patient samples exhibiting high (left panels) or low (right panels) staining for pT328-PKM2. f The GBM patient cohort (n = 104) was separated into two groups along the median pT328-PKM2 H-score. Survival was analyzed by the Kaplan Meier method. Statistical differences in overall survival between the groups were determined by the log rank test (P = 0.04). *P < 0.05