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Fig. 3 | Genome Biology

Fig. 3

From: Functional genomics analyses of RNA-binding proteins reveal the splicing regulator SNRPB as an oncogenic candidate in glioblastoma

Fig. 3

SNRPB impacts cancer-relevant processes. a Cellular viability was assayed by MTS and shows that SNRPB knockdown caused a significant reduction of viability in U251 (p-value = 0.002; Wilcoxon rank-sum test) and U343 cells (p-value < 0.001; Wilcoxon rank-sum test), compared to control transfected cell lines (siCtrl). b Caspase-3/7 assay shows an increase in apoptosis in siSNRPB compared to siCtrl in both cell lines (U251 p-value = 0.011; U343 p-value = 0.007; Wilcoxon rank-sum test). c Plots show confluence percentage monitored by IncuCyte over 96 hours, comparing siSNRPB with siCtrl. Proliferation reduction was observed in both cell lines upon SNRPB knockdown (U251 p-value < 0.001; U343 p-value < 0.001; ANOVA). Right panel shows U251 cellular profile at time zero and after 96 hours of transfection with siCtrl and siSNRPB. SNRPB knockdown resulted in a strong reduction in cell proliferation compared to control. d Downregulation of SNRPB by siRNA leads to inhibition of cell growth and cell detachment in two glioma stem cell lines. The percentage of the normalized cell index was calculated with respect to control. Results represent an average of two (line 326) or three (line 83) [39] individual experiments and each experiment was done in triplicate. Red arrowheads indicate the floated round up cell colonies on the plates where SNRPB siRNA was transfected. e SNRPB expression in mouse neural stem cells (NSCs) was compared to differentiated neural cells after 4 days by RNA-Seq. SNRPB expression was higher in undifferentiated cells (log2 fold change = 0.599347, FDR-adjusted p-value < 0.05)

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