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Supplementary data from Circulating Tumor Microparticles Promote Lung Metastasis by Reprogramming Inflammatory and Mechanical Niches via a Macrophage-Dependent Pathway
Supplementary Figure S1. Size distribution of T-MPs isolated from hypoxic or normoxic tumor cells. Supplementary Figure S2. Analysis of lung metastasis and overall survival after tail vein injection of 4T1 breast cancer cells in mice pretreated with 4T1-MPï¼ŒS-MP or PBS. Supplementary Figure S3. Confocal microscopic analysis of PKH26-MPs in lung. Supplementary Figure S4. Analysis of lung endothelial permeability. Supplementary Figure S5. The proportion of T cells, B cells and NK cells in the lungs were analyzed by flow cytometry after treatment of with 4T1-MPï¼ŒS-MP or PBS. Supplementary Figure S6. CCL2 was mainly produced by lung macrophages that had taken up T-MPs. Figure S7. DNA fragments in hypoxic tumor cell-MPs contribute to macrophages upregulating CCL2 expression via the cGAS/STING/STAT6 pathway. Supplementary Figure S8. CCL2-attracted monocytes transit to macrophages. Supplementary Figure S9. F4/80+CD11b+Ly6C- macrophages effectively inhibited OVA257-264 peptide-stimulated OT-1 T cell proliferation in vitro and in vivo. Supplementary Figure S10. T-MP-induced VEGF production by macrophages contributes fibrin deposition in the lungs.