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. 2021 Dec 22;12:754196. doi: 10.3389/fimmu.2021.754196

Figure 3.

Figure 3

MDSCs promote angiogenesis and induce cancer stem cells (CSCs) in the TME. MDSCs contribute to tumor vascularization by producing high levels of matrix metalloproteinase 9 (MMP9). MDSCs directly produce angiogenic factors, including VEGF and bFGF through Stat3 activation to induce angiogenesis. MDSCs control the expression of CD31 and CD117 through the expression of the Wilms’ tumor suppressor Wt1, causing tumor vascularization. MDSCs shift the IFNγ/IL6 balance to promote neovascularization through IDO1 signaling. MDSCs-secreted S100A8 and S100A9 stimulate angiogenesis. Exosomes miR-126a released from MDSCs promote tumor angiogenesis. MDSCs differentiate into endothelial cells (ECs). MDSCs endow stem-like qualities to breast cancer cells through IL6/STAT3 and NO/Notch cross-talk signaling and to epithelial ovarian cancer (EOC) cells by the colony-stimulating factor 2 (CSF2)/p-STAT3 signaling pathway. MDSCs also trigger the expression of miRNA101 and piRNA-823 to promote the stemness of ovarian carcinoma cells and myeloma (MM) cells, respectively. MDSCs can indirectly modulate the stemness of tumor cells through the secretion of various factors such as exosomal S100A9, TGF-β1, PGE2, MMP9, and chitinase 3-like 1 (CHI3L1).