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Fig. 1 | Stem Cell Research & Therapy

Fig. 1

From: Mesenchymal stem cells in preclinical cancer cytotherapy: a systematic review

Fig. 1

Mechanisms of MSC homing to tumor sites. Binding of monocyte chemotactic protein-1 (MCP-1 or CCL2), secreted by breast cancer cells or of stromal cell-derived factor 1 (SDF-1) secreted by breast, colon, and prostate cancer cells, on their receptors expressed on MSC surface can modulate the tropism of MSC to tumor sites. Matrix metalloproteinase 1 (MMP-1), localized in the extracellular matrix (ECM), stimulates MSC homing through cleavage and subsequent activation of the G-protein protease-activated receptor (PAR)-1. In correspondence with the homing process of MSC to sites of injury, the interaction between integrin α4/β1 on MSC and its binding site on fibronectin of the ECM plays a major role in the transmigration of MSC into the extracellular matrix. Finally, MSC recruitment can also be achieved through interaction of VEGF, secreted by cancer cells, with its receptor on MSC. After incorporating in tumor site, MSC in turn secrete various pro-angiogenic factors, such as VEGF, fibroblast-derived growth factor, PDGF, and SDF-1 that facilitate angiogenesis

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