Supplemental Figures S1-S14 from Forced Activation of Notch in Macrophages Represses Tumor Growth by Upregulating miR-125a and Disabling Tumor-Associated Macrophages

Figure S1: Expression of Notch ligands and receptors in macrophages during in vitro differentiation and activation. Figure S2: Activation of Notch signaling in macrophages repressed the growth of transplanted B16F melanoma tumors. Figure S3: Activation of Notch signaling by conditional NIC expression in macrophages did not change the number of macrophages, but reduced the number of MDSCs and increased the number of CD8+ T-cells in transplanted tumors. Figure S4: miR-125a expression in BM cells and macrophages. Figure S5: miR-125a is a downstream molecule to Notch signaling in macrophages. Figure S6: Activation of Notch signaling with immobilized mD1R in macrophages promoted M1 polarization. Figure S7: Characterization of the miR-125a gene and its enhancer. Figure S8: The sequence of the first intron enhancer of Spaca6A. Figure S9: miR-125a enhanced phagocytosis of differentially activated macrophages. Figure S10: Notch signaling regulated M1 and M2 macrophage polarization. Figure S11: miR-125a regulated M1 macrophages through targeting FIH1. Figure S12: miR-125a repressed M2 macrophages through targeting IRF4. Figure S13: Self-amplification of miR-125a expression through RYBP/YY1. Figure S14: A model of the Notch signaling-mediated regulation of TAMs through miR-125a.