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. 2020 Aug 6;5(15):e134290. doi: 10.1172/jci.insight.134290

Figure 6. Association of MEK activation with CXCR1/CXCR2 ligands in cancer cell lines and human breast tumors.

Figure 6

(A) Correlation of select cytokine mRNAs with the Ras/MAPK pathway activation gene signature score across 50 breast cancer cell lines in the CCLE. CXCL1, CXCL2, CSF1, CSF2, and CXCL8 gene expression were all significantly associated with Ras/MAPK activity (P < 0.0001 for all), while CXCR3 (T cell–recruiting) chemokines were not associated with Ras/MAPK activity. (B) CXCR1/2 (MDSC-recruiting) chemokines were positively associated with Ras/MAPK activation in human TNBC (TCGA). CSF family members 1 and 3 were positively associated with Ras/MAPK activation in human TNBC (TCGA). CXCL9, CXCL10, and CXCL11 (CXCR3 ligands/T cell–recruiting chemokines) were negatively associated with Ras/MAPK activation in human TNBC (TCGA). (C) Representative quantitative immunofluorescence analysis for HLA-DR (shown in yellow), CD11b (red), and pan-cytokeratin (green) with DAPI as nuclear counterstain. Original magnification, ×200. (D) Correlation of Ras/MAPK transcriptional score versus CD11b+HLA-DR– (immunosuppressive myeloid cells) expressed as a percentage of all CD11b+ cells across 61 TNBCs after neoadjuvant chemotherapy (6, 21). Data were assessed in tissue microarray format, using the average cell number across 3 independent cores per patient sample.