Fig. 5

KDM2A-expressed fibroblasts stimulated CCL2 released from macrophage through CXCR2 to increase the paclitaxel resistance in breast cancer. A PMA-pretreated THP-1 was treated with 100 ng/ml CXCL2, CXCL5, or IL-8, and relative mRNA and protein levels of CCL2 were determined by Real-time PCR and western blot analysis. B PMA-pretreated THP-1 cells were incubated with RMF-CM or K2A-CM in the presence and absence of CXCR2 inhibitor SB225002 (25 nM). Relative mRNA and protein levels of CCL2 were analyzed by Real-time PCR and western blot analysis. C Cell viability analysis of paclitaxel-treated HS-578 T cells. HS-578 T cells were treated with conditioned medium TRMF-CM or TRK2A-CM supplemented with additional 25 nM paclitaxel for 48 h. D Cell viability of paclitaxel-treated HS-578 T cells co-treated with TRK2A-CM in the presence and absence of CCR2 inhibitor INCB3344 (5 nM) for 48 h. Cell viability was determined and counted using the trypan blue exclusion assay. Each experiment was performed in triplicate and was repeated three times independently. Differences were found to be statistically significant at * p < 0.05, **p < 0.01, and ***p < 0.001