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Table 1 The effect of MSC-derived mediators on tumor growth

From: Mesenchymal stem cells as a double-edged sword in tumor growth: focusing on MSC-derived cytokines

Pro-tumorigenic activity of MSCs Factors secreted by Effects of secreted factors and mediators References
Immunosuppression MSCs: TGFβ, IFNγ, TNFα, PGE2, CCL2, galectin-9, HGF, CTLA-4, soluble PD-L1 and PD-L2, NO, HLA-G, IDO, IL-1α, IL-1β, IL-4 and IL-6 Immune tolerance
T, B, NK, Dendritic cell inhibition
Promotion of Treg cells proliferation
Recruitment of MDSCs
Apoptosis of lymphocytes and neutrophils
Reduction of CD80/CD86 expression on APCs
[40, 92,93,94,95,96, 103,104,105, 109]
Promotion of angiogenesis VEGF, FGF-2, βFGF, PDGF, IL-6, IL-8, TGFβ and angiopoietin-1 Promotion of tumor angiogenesis
Transformation into smooth muscle cells and pericytes
Mobilization and recruitment of MSCs into neovascularization sites
Tumor vessel formation
Inducing expressing of junctional proteins
[51, 88, 123, 124, 127,128,129, 135,136,137]
Transition of mesenchymal stem cells to cancer-associated fibroblasts CAFs: α-SMA, tenascin-C, fibroblast surface protein (FSP), CCL5, CXCL12, IL-6, IL-4, IL-8, TNF, TGFβ, VEGF Stimulation of tumor growth
Promotion of tumor vascularization
[88, 142,143,144]
Epithelial–mesenchymal transition (EMT) HGF, EGF, PDGF, leptin and TGFβ Induction of transcriptional regulators: snail, slug, twist, Zeb1
Increasing the metastatic capacity
Inducing EMT and promoting a cancer stem cell (CSC) phenotype
[152,153,154, 157, 158]
Correlation of MSCs with cancer stem cells BMP, IL-6, IL-8, CXCL6, and CXCL5 Proliferation of CSCs and increasing their invasive properties [90, 164, 165]
Promotion of tumor metastasis Lysyl oxidase (LOX), TGFβ, FGF, HGF, EGF, CCL5, CXCL5, CXCL1, CXCL7 and CXCL8 Promotion of tumor cell migration
Extracellular matrix modulation
Enhancing tumor cell invasiveness and inducing EMT
Activation of matrix metalloproteinase 9 (MMP-9)
Overexpression of rho-associated kinase
[59, 75, 167, 171, 173,174,175]
Inhibition of apoptosis in cancer cells VEGF, FGF-2, PDGF, HGF, BDNF, SDF-1α, IGF-1 and IGF-2, TGF-β and IGFBP-2 Inhibition of tumor cell apoptosis and promotion of tumor proliferation
Stimulation of the angiogenesis
[52, 184,185,186,187,188]
Promotion of drug resistance CXCL12, EGF, IGF, IL-6, IL-7, IL-8 and PGE-2 Reducing caspase 3 activity
Inhibition of apoptosis following cytotoxic therapy
Promotion of the CSCs formation
[91, 133, 164, 196, 198]