Fig. 2: Sema3C promotes GSC self-renewal.
From: Sema3C signaling is an alternative activator of the canonical WNT pathway in glioblastoma
a, b Left panels: representative tumorsphere images of 387 (a) and 4121 (b) GSCs after control shNT, shSema3C#1, and shSema3C#2 knockdown. Scale bar 100 μM. Right panels: quantification of tumorspheres after Sema3C knockdown (n = 4 biological replicates in each group, compared with control unadjusted p < 0.0001, error bars: S.D. Scale bar 100 μM). c, d In vitro extreme limiting dilution assay in Sema3C knockdown 387 GSCs (c) and 4121 GSCs (d). Tables show estimated stem cell frequencies in control shNT, shSema3C#1, and shSema3C#2 knockdown GSCs with 95% confidence intervals (n = 24 replicates in each dose, compared with control unadjusted p < 0.0001, error bars: S.D.). e, f Left panels: representative immunofluorescence images of EdU incorporation assay in 387 (e) and 4121 (f) GSCs after control shNT, shSema3C#1, and shSema3C#2 knockdown. Right panels: quantification of EdU+ cells over total cells (EdU in red, DAPI in blue, n = 3 independent experiments, 387 GSCs control vs. shSema3C#1 unadjusted p = 0.0002; control vs. shSema3C#2 unadjusted p = 0.0006. 4121 GSCs control vs. shSema3C#1 unadjusted p < 0.0001; control vs. shSema3C#2 unadjusted p = 0.0053, error bars: S.D. Scale bar 50 μM). g, h Cell viability of 387 and 4121 GSCs after Sema3C knockdown (n = 6 biological replicates for each group, compared with control unadjusted p < 0.0001, error bars: S.D.). Source data are provided as a Source data file.
