Gene expression data from colorectal cancers

D122p53 mice (a model of D133p53 isoform) are tumour prone, have extensive inflammation and elevated serum IL-6. To investigate the role of IL-6 we crossed ∆122p53 mice with IL-6 deficient mice. Here we show that loss of IL-6 reduced JAK-STAT signalling, tumour incidence, and metastasis. We also show that D122p53 activates RhoA-ROCK signalling leading to tumour cell invasion which is IL-6 dependent and can be reduced by inhibition of JAK-STAT and RhoA-ROCK pathways. Similarly, we show that Δ133p53 activates the these pathways, resulting in invasive and migratory phenotypes, in colorectal cancer cells. Gene expression analysis of colorectal tumours showed enrichment of GPCR signalling associated with D133TP53 mRNA. Patients with elevated D133TP53 mRNA levels had a shorter disease free survival. Our results suggest that D133p53 promotes tumour invasion by activation of the JAK-STAT and RhoA-ROCK pathways and that patients whose tumours have high D133p53 may benefit from therapies targeting these pathways. In this dataset, we included the gene expression data from 35 colorectal cancers. These data were used to identify a list of enriched genesets associated with D133TP53 mRNA expression in colorectal tumours D133TP53 mRNA expression determined by RT-qPCR was combined with transcript level data from Affymetrix Human Exon 1.0 ST arrays for the 35 colorectal tumours. Using Spearman's correlation analyses we identified D133TP53 mRNA was associated with the expression of 364 genes (Spearman’s correlation coefficient r ≥ 0.35). Enrichment of gene sets within the input list was determined using the overrepresentation test with default settings using Bonferroni correction in Pantherdb