Figure 5.

CXCL1 induced radioresistance in GBM via regulation of NF‐κB signaling and mesenchymal transition. A, Hierarchical bi‐clustering analysis was performed by using TCGA GBM database, indicating the significant gene signature in CXCL1^high GBM compared with CXCL1^low GBM. B, The amount of differentially expressed genes in CXCL1^high and CXCL1^low groups was presented by volcano plot (log₂FC > 1 or log₂FC<−1, with an adjusted P value < .05). C, Gene ontology (GO) analysis for differentially expressed genes. (CXCL1^high vs CXCL1^low).D and E, Gene set enrichment analysis (GSEA) was performed to find out the highly enriched signaling pathways in CXCL1^high group. F, mRNA expression of NF‐κB was measured by qRT‐PCR analysis (***P < .001, with t test). G, Western blot of total NF‐κB/p65 expression, β‐actin was used as a loading control. H, mRNA expression of mesenchymal transition markers was measured by qRT‐PCR analysis (**P < .05, with one‐way ANOVA followed by Dunnett's post‐test). I, Western blot of mesenchymal transition markers. β‐actin was used as a loading control