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. 2016 Jun 20;126(7):2757–2772. doi: 10.1172/JCI86114

Figure 1. NOTCH inhibition does not attenuate cell autonomous BTIC growth.

Figure 1

(A) Left: Matched sets of BTICs and non-BTICs (387, 3691, and 4121) were transfected with a 4× RBPJ luciferase reporter together with a tk-renilla reporter. Data are displayed as mean ± SEM for the ratio of firefly-to-renilla luciferase (t test, **P < 0.01, n = 3). Right: 3691 and 4121 BTICs were transfected with a 4× RBPJ luciferase reporter together with a tk-renilla reporter, and then treated with the NOTCH antagonist, DAPT (5 μM), or vehicle control (DMSO). Data are displayed as mean ± SEM for the ratio of firefly-to-renilla luciferase (Student’s t test, **P < 0.01, n = 3). (B) Effects of DAPT or vehicle control (DMSO) on cell proliferation were tested in two BTIC models (3691 and 4121). Data are displayed as the mean values for each time point. (C) Cleaved NOTCH1 (NOTCH intracellular domain [NICD]) levels were analyzed by immunoblot after treatment with vehicle control or DAPT in two BTIC models (3691 and 4121). (D) Effects of the stapled peptide NOTCH inhibitor, SAHM1, or vehicle control (DMSO) on cell proliferation were tested in two BTIC models (3691 and 4121). Data are displayed as the mean values for each time point. (E) Effects of SAHM1 treatment on downstream NOTCH target gene expression (HES1 and HES5) were tested in two BTIC models (3691 and 4121). Cells were treated with SAHM1 for two days. Total RNA was isolated and cDNA was synthesized by reverse transcription. The mRNA levels of indicated genes were detected by qPCR (t test, *P < 0.05, n = 3).