Fig. 2

CXCR2 knockout decreases melanoma tumor burden. a Tyr-Cre^ER+:: Braf^CA/+::Pten^{lox4−5/lox4−5}::mT/mG C57BL/6 mice were crossed with floxed Cxcr2 mice to obtain mice with inducible tumors with or without CXCR2 expression. Thirty-six days after 4-HT administration, skin tumor volume and count were recorded, and mice were photographed (significance determined by Welch's t-test). Similarly, b Tyr-Cre^ER+::NRas^Q61R::Ink4a^−/− mice were crossed with floxed Cxcr2 mice, and resulting pups were treated with 4-HT on days 1 and 2 prior to UV irradiation on day 3 to initiate tumor formation (n = 16/genotype). Tumors were measured, counted, and mice were photographed (significance determined by Welch's t-test). RNA was extracted from Braf^V600E/Pten^−/−/Cxcr2^−/− and Braf^V600E/Pten^−/−/Cxcr2^WT tumors and subjected to RNAseq analysis. c A volcano plot showing fold change and significance of differential gene expression in Cxcr2^−/− tumors compared to Cxcr2^WT tumors. d Gene set enrichment analysis (GSEA) of RNAseq data identifies 8 gene sets enriched in Cxcr2^−/− tumors. Point size indicates the gene ratio (percent of genes from the gene set contributing to the enrichment score) and point color represents the FDR q-value