RelB acts as a molecular switch driving chronic inflammation in glioblastoma multiforme

We observed that RelB stimulates the production of IL-1B, IL-6 and COX2 in GBM cells, whereas RelB inhibits the production of IL-1B, IL-6, and COX2 in astrocytes. Given these data we hypothesized that RelB signaling acts as a molecular switch to induce chronic inflammation in GBM. While we had demonstrated this differential control of IL-1B, IL-6 and COX2 expression in GBM cells and astrocytes, we sought to define the global role of RelB in response to inflammatory cytokines. In order to define the global role of RelB in response to inflammation in GBM, we stimulated both parental and RelB (-/-) cells with IL-1B/OSM, performed RNAseq, and conducted differential expression testing and pathway enrichment between the two groups.