Fig. 1: The expression of NEK2 is significantly upregulated in GBM patients.
From: NEK2 enhances malignancies of glioblastoma via NIK/NF-κB pathway
A Gene expression analysis in GBM versus nontumor by using TCGA database (*P < 0.001, with student’s t-test). B Gene expression analysis with TCGA database in different WHO grades of glioma (*P < 0.001, with student’s t-test). C Gene expression analysis with REMBRANDT databases in different WHO grades of glioma (*P < 0.001, with student’s t-test). D Gene expression analysis with GRAVENDEEL databases in different WHO grades of glioma (*P < 0.001, with student’s t-test). E Gene expression analysis for primary GBM and recurrent GBM by using TCGA database. F Representative IHC images of NEK2 in glioma samples. Brain tissue from epilepsy surgery was used as negative controls. G Gene expression analysis in contrast-enhancing GBM, nonenhancing GBM and nontumor by using GILL25114226 database. H Kaplan-Meier OS analysis for NEK2 expression by using GBM patient samples (*P = 0, with log-rank test). I Kaplan-Meier DFS analysis for NEK2 expression by using GBM patient samples (*P < 0.001, with log-rank test). J NEK2 mRNA expression in human primary glioma cell, commercial human glioma cell lines and NHA by qRT-PCR (**P < 0.01, *P < 0.05, with one-way ANOVA followed by Dunnett’s post-test). G Western blot analysis was conducted to detect the protein levels of NEK2 in human primary glioma cell, commercial human GBM cell lines and NHA. β-actin was set as an internal control. All data were reported as the mean ± SD of triplicate independent experiments.
