Abstract
The discovery of tissue reparative and immunosuppressive abilities of mesenchymal stem cells (MSCs) has drawn more attention to tumor microenvironment and its role in providing the soil for the tumor cell growth. MSCs are recruited to tumor which is referred as the never healing wound and altered by the inflammation environment, thereby helping to construct the tumor microenvironment. The environment orchestrated by MSCs and other factors can be associated with angiogenesis, immunosuppression, inhibition of apoptosis, epithelial-mesenchymal transition (EMT), survival of cancer stem cells, which all contribute to tumor growth and progression. In this review, we will discuss how MSCs are recruited to the tumor microenvironment and what effects they have on tumor progression.
Highlights
Mesenchymal stem cells (MSCs, called as mesenchymal stromal cells) is a subset of non-hematopoietic adult stem cells which originate from mesoderm
Current data suggested that mesenchymal stem cells (MSCs) promoting tumor angiogenesis was mainly dependent on their differentiation potential into endothelial-like cells or pericytes and secreting proangiogenic factors like vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), fibroblast growth factor (FGF) and CXCL12, thereby facilitating angiogenesis [1]
This review draws attention to the complex of MSCs interaction with tumor microenvironment and highlights the fact that both tumor growth and tumor metastasis can be influenced by MSCs directly or indirectly
Summary
Mesenchymal stem cells (MSCs, called as mesenchymal stromal cells) is a subset of non-hematopoietic adult stem cells which originate from mesoderm. Current data suggested that MSCs promoting tumor angiogenesis was mainly dependent on their differentiation potential into endothelial-like cells or pericytes and secreting proangiogenic factors like vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), fibroblast growth factor (FGF) and CXCL12, thereby facilitating angiogenesis [1]. MSCs were reported to suppress B cell function via inhibiting chemokine receptors expression [141], to prevent the maturation and cytokine production of DCs and to decrease IL-2 induced proliferation, cytokine production and cytotoxic activity of NK cells. Nitric oxide (NO), as another important molecule secreted by MSCs, was considered as a bifunctional regulator of apoptosis, proapoptotic at high dose and antiapoptotic at low [152] Another essential chemokine IL-6 produced by tumor cells and MSCs inhibit apoptosis by upregulating the expression of Bcl-xl [153]. Further researches gave the indication that CCL5 produced by tumor cell-stimulated MSCs, through binding with CCR5, lead the tumor metastasis [156]
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