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. 2016 Oct 6;7(43):69173–69187. doi: 10.18632/oncotarget.12507

Figure 6. TGF-β is one source of NF-κB activation in GBM.

Figure 6

A. 6969 and GBM6 explants were stimulated with 10ng/mL TGF-β for 6 or 24 hours, then analyzed by immunoblotting for phosphorylation of Smad and p65. B. 6969 and GBM6 explants were treated with 10 μM SB431542, a TGF-βR1 inhibitor, for 6 or 24 hours, then analyzed by immunoblotting for p65 phosphorylation. C. 6969 or 7030 cells were transfected with 3x-κB luciferase reporter and treated with DMSO or 10 μM SB431542 for 24 hours, then harvested and analyzed for luciferase activity (n = 3, **p < 0.0001, *p < 0.01 by t-test, error bars represent SEM). D. Quantification of tumorsphere formation in GBM6 CD133+ cells following treatment with 10 μM SB431542 either once or daily. Data are represented as the mean ± SEM, **p < 0.0001 by t-test.