CXCR4 Antibody - #AF5279

Fig. 5 Characterizing endothelial cell subsets within the tumor microenvironment of breast cancer. A Single-cell map showing endothelial cell subsets. B UMAP plots of 1425 endothelial cells from eight patient samples. C UMAP showing single-cell profiles of endothelial cells in the angiogenic and non-angiogenic groups. D Endothelial cell subcluster composition for different patients. E Scatter plot showing differences in the distribution of endothelial cell subclusters between angiogenic negative and positive groups. The ecology of angiogenic and non-angiogenic breast cancer groups. F–G Violin plot and UMAP figure showing the expression of markers related to angiogenesis and exosomes in these endothelial cell subsets and individual distribution. H Immunofluorescence images of CXCR4, S100A9 and PPP1R1B expression, which are highly specific in the angiogenesis group and distribution of marker genes. Scale bar, 20 µm. I Representative IHC images of gene signatures

Fig. 1: The siRNA-KDM6B inhibited the migration of BMSCs in vitro. A The knockdown efficiency of KDM6B was verified by qRT-PCR. B, C The siRNA-KDM6B inhibited the protein expression of migration-related genes (N cadherin and CXCR4). D, E The IF showed the expression of CXCR4 was inhibited by siRNA-KDM6B. F, G The siRNA-KDM6B inhibited the actin cortical protrusions formation of BMSCs. H, I The scratch test showed that siRNA-KDM6B decreased the migration area of BMSCs. J, K Transwell test verified that siRNA-KDM6B inhibited the migrated MSCs number. (si-1: siKDM6B-1, si-2: siKDM6B-2, si-3: siKDM6B-3. *P 

Fig. 3. Long-term expression efficiency of CXCR4 and CXCR7 in UCMSCs after lentiviral vector transduction. (a) The UCMSCs transduced separately with pHBLV-CMVIE-ZsGreen-T2A-puromycin (UCMSCsOE-NC), pHBLV-CMVIE-CXCR4-ZsGreen-T2A-puromycin (UCMSCsOE-CXCR4) and pHBLV-CMVIE-CXCR7-ZsGreen-T2A-puromycin (UCMSCsOE-CXCR7) lentiviral vectors were cultured for 20 passages and observed by light microscopy (top) and fluorescence microscopy with a green fluorescent protein (bottom), 100×. (b) At passage 20 after transduction, the immunophenotype of UCMSCsOE-CXCR7 was analyzed by flow cytometry. Adherent UCMSCs were positive for CD29, CD73, CD105 and CD166 but negative for CD11b, CD34, CD45 and HLA-DR. Isotype-matched controls were used for comparison. Immunophenotype analysis of UCMSCs and UCMSCsOE-CXCR4 by flow cytometry is described in Supplementary Figure 1b-c (Fig. 1S b-c). (c) Determination of CXCR7 mRNA expression in UCMSCs by qRT-PCR analysis after pHBLV-CMVIE-ZsGreen-T2A-puromycin, pHBLV-CMVIE-CXCR4-ZsGreen-T2A-puromycin and pHBLV-CMVIE-CXCR7-ZsGreen-T2A-puromycin transduction. (d) Western blot analysis showed increased CXCR7 and CXCR4 protein expression in transduced UCMSCs. * ** *p 

Figure 6 Downregulation of c-Myc enhanced the antitumor effect of bufalin in pancreatic cancer cells through the HIF-1α/SDF-1/CXCR4 pathway. (A) The protein expression of c-Myc, vimentin, E-cadherin, HIF-1α, CXCR4, and SDF-1 in PANC-1 and SW1990 pancreatic cancer cells under different treatments was detected via western blot. (B) Quantification results of protein expressions of c-Myc, vimentin, E-cadherin, HIF-1α, CXCR4, and SDF-1 in PANC-1 pancreatic cancer cells. (C) Quantification results of protein expression of c-Myc, vimentin, E-cadherin, HIF-1α, CXCR4, and SDF-1 in SW1990 pancreatic cancer cells (* p < 0.05, ** p < 0.01 vs control, ▲ p < 0.05, ▲▲ p < 0.01 vs bufalin treatment group, n = 3).