Skip to main content
. 2020 Nov 3;143(11):3273–3293. doi: 10.1093/brain/awaa273

Figure 7.

Figure 7

Inhibition of the PDGF-PDGFRB pathway as potential driver of the SRSF3 silencing-induced anti-glioblastoma tumour actions. (A) Expression levels (mRNA levels measured by nCounter PanCancer and protein levels measured by western blot) of different components of the PDGFRB activated pathways (in bold) in SRSF3 siRNA-transfected versus scramble-transfected U-87 MG-induced xenograft tumour samples (n = 4). (B) Phosphorylated protein ratios and total protein levels of AKT and ERK in SRSF3-silenced U-87 MG and U-118 MG cells compared to scramble-controls (n = 5) after 24 h of silencing. (C) Proliferation rates after treatment with PDGFDD homodimer (specific PDGFRB ligand) on scramble-transfected versus SRSF3-silenced U-87 MG, U-118 MG cells and primary patient-derived glioblastoma cells (n = 3). (D) Number of cells per tumoursphere and representative images of formation of tumorspheres after treatment with PDGFDD homodimer (specific PDGFRB ligand) on scramble-transfected and SRSF3-silenced U-87 MG and U-118 MG cells (n = 6). (E) Phosphorylated ratio of AKT/ERK after treatment with PDGFDD homodimer (specific PDGFRB ligand) on scramble-transfected U-87 MG cells versus SRSF3-silenced U-87 MG (n = 5) and U-118 MG cells (n = 4). Data represent means ± SEM. *P, 0.05; **P, 0.01; ***P, 0.001, significantly different from control conditions. #P, 0.05; ##P, 0.01; ###P, 0.001, significantly different from Scramble+PDGFDD condition. See also Supplementary Fig. 9.