Figure 5

NTS induced the activation of Erk1/2 through NTSR1 in GL261 glioma cells. A, GL261 glioma cells were stimulated with 50 nM NTS for the indicated times. B, Glioma cells were stimulated with NTS at indicated concentrations for 5 min. C, GL261 glioma cells were stimulated with NTS for 5 min in the absence or presence of 5 μM SR48692 or 2 ng/ml NTS-NA. *p < 0.01 vs. the control group, ^# p < 0.01 vs. the 100 nM NTS-stimulated group. D, GL261 glioma cells were stimulated with NTS for the indicated times in the presence of Sc-siRNA or NTSR1-siRNA. *p < 0.01 vs. the 100 nM NTS-stimulated group in the presence of Sc-siRNA for 2 min, ^# p < 0.01 vs. the 100 nM NTS-stimulated group in the presence of Sc-siRNA for 5 min. The cell lysates were evaluated by western blot analysis using antibodies against phospho-Erk1/2. The results were standardized to the total levels of Erk2 and are expressed as the mean ± SEM from at least three independent experiments. E and F, The percentages of BrdU-positive cells and invasived cells in the presence of SR48692 and the MEK1/2-selective inhibitor U0126. *p < 0.01 vs. the control group, ^# p < 0.01 vs. the control group.