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Figure 4: Influence of FL34 on HH signaling pathway activity. (a) GLI1 inhibitory activity of FL34 measured by a dual luciferase reporter assay. The GLI1 activity was inhibited following the administration of FL34 for 48 h. The error bars represent the standard deviation. *P < 0.05 versus control cells. (b) The effect of FL34 on the level of GLI1 in U-87 MG and T98G cells analyzed by reverse transcription-quantitative polymerase chain reaction. Data were normalized to GAPDH expression. Quantitative data are expressed as the mean ± standard deviation. *P < 0.05, **P < 0.01, and ***P < 0.001 versus control. (c) The effect of FL34 on the HH signaling pathway in U-87 MG and T98G cells analyzed by western blotting. Cells were treated with the indicated concentrations of FL34 for 72 h. “Con” refers to untreated control samples. Whole-cell lysates were subjected to western blotting with antibodies against the indicated proteins; western blotting for β-actin was used as a loading control. Representative western blot images are presented for each experiment. (d) The effect of FL34 on the HH signaling pathway in U-87 MG xenograft tumors. Mice bearing U-87 MG tumors were randomized and treated with FL34 15.0 or 30.0 mg/kg FL34 daily for 14 days. Left panel, GLI1 mRNA levels in U-87 MG xenograft tumors. The error bars represent the standard deviation, **P < 0.01. Right panel lysates of two or three mice from each group were pooled. Each lane represents one protein pool, and two or three pools/group was subjected to western blot analysis. β-actin was included as a loading control. The blots were incubated with the indicated antibodies. Representative blots are presented

Figure 4: Influence of FL34 on HH signaling pathway activity. (a) GLI1 inhibitory activity of FL34 measured by a dual luciferase reporter assay. The GLI1 activity was inhibited following the administration of FL34 for 48 h. The error bars represent the standard deviation. *<i>P</i> < 0.05 versus control cells. (b) The effect of FL34 on the level of GLI1 in U-87 MG and T98G cells analyzed by reverse transcription-quantitative polymerase chain reaction. Data were normalized to GAPDH expression. Quantitative data are expressed as the mean ± standard deviation. *<i>P</i> < 0.05, **<i>P</i> < 0.01, and ***<i>P</i> < 0.001 versus control. (c) The effect of FL34 on the HH signaling pathway in U-87 MG and T98G cells analyzed by western blotting. Cells were treated with the indicated concentrations of FL34 for 72 h. “Con” refers to untreated control samples. Whole-cell lysates were subjected to western blotting with antibodies against the indicated proteins; western blotting for β-actin was used as a loading control. Representative western blot images are presented for each experiment. (d) The effect of FL34 on the HH signaling pathway in U-87 MG xenograft tumors. Mice bearing U-87 MG tumors were randomized and treated with FL34 15.0 or 30.0 mg/kg FL34 daily for 14 days. Left panel, GLI1 mRNA levels in U-87 MG xenograft tumors. The error bars represent the standard deviation, **<i>P</i> < 0.01. Right panel lysates of two or three mice from each group were pooled. Each lane represents one protein pool, and two or three pools/group was subjected to western blot analysis. β-actin was included as a loading control. The blots were incubated with the indicated antibodies. Representative blots are presented