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Fig. 2 | Journal of Biomedical Science

Fig. 2

From: Enrichment of superoxide dismutase 2 in glioblastoma confers to acquisition of temozolomide resistance that is associated with tumor-initiating cell subsets

Fig. 2

The resistant features in cell lines were related to increased SOD2 expression. a Cell density assay of the parental and resistant U87MG and A172 cells with SOD2 knockdown or empty vector (EV) control groups. The cells were treated with TMZ in dose-dependent manner for 72 h. b Clonogenic assay of the resistant cell lines with stable SOD2 knockdown. TMZ was given after cell attached, incubated for 72 h and then changed to drug-free medium for colony to form. The bar graphs showed the ratio of TMZ-treated groups to the untreated control of their own cells. c Cell density assay of the parental cell lines with overexpression of SOD2. The cells were treated with TMZ in dose-dependent manner for 72 h. d The basal level of SOD2 activity was examined in the parental and the resistant U87MG. The bar graph represented mean values of triplicate experiment. e The TMZ-induced mitochondrial ROS were detected with MitoSox in parental and resistant U87MG cells. The mean fluorescent intensity (MFI) gated by the control was calculated into the ratio over the parental cells. The average of triplicate experiment was shown in the bar graphs. f The caspase 3 expression was detected in the resistant cell lines after TMZ incubation for 24 h. Transfection with SOD2 siRNA was done 72 h before TMZ treatment. g Survival curves of the orthotopic mouse model in which mice were implanted with lentiviral empty vector (EV)- or SOD2 shRNA-infected resistant A172 cells (n = 8 for each group). Treatment with TMZ or vehicle was administered daily, five days a week (P = 0.001 in the SOD2 shRNA groups, P > 0.05 in the EV groups). (*P < 0.05; N.S., non-significant)

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