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. 2019 Oct 21;22(3):333–344. doi: 10.1093/neuonc/noz204

Fig. 2.

Fig. 2

Expression of ICOSLG is regulated by NF-κB. (A)FACS analysis of ICOSLG expression in 146 PN GSCs after 96 h of treatment with 10 ng/mL TNF-α. GSCs were stained with isotype control (green histograms) or ICOSLG-specific (purple histogram) antibodies. The numbers in each panel indicate the MFI-R. (B) MFI-R of ICOSLG-expressing PN GSCs (146, 157, 528) analyzed after stimulation with proinflammatory cytokines (IL-1β, IFN-γ, or TNF-α) for 96 h (A). Data are expressed as the means ± standard error of three independent experiments (*P < 0.05, PN GSCs [n = 3] vs. PN GSCs + proinflammatory cytokines [n = 3], one-way ANOVA). (C) Luciferase-reported NF-κB activity was measured in MD13 (MES) and 146 (PN) GSCs. Data represent the means ± standard deviation (*P < 0.01, n = 3). (D)Silencing NF-κBp65 significantly attenuated ICOSLG expression with TNF-α treatment. Data are expressed as the means ± standard error of 3 independent experiments (*P < 0.05, PN GSCs [n = 3] vs. PN GSCs + siNF-κBp65 [n = 3], one-way ANOVA). (E) PN GSCs (146, 157, 528) were grown in 1% oxygen for 48 h, and the level of ICOSLG was determined with flow cytometry. Data are expressed as the means ± standard error of 3 independent experiments (*P < 0.05, PN GSCs [n = 3] vs PN GSCs + hypoxia [n = 3], one-way ANOVA).