Abstract
Mesenchymal stem cells (MSCs) can exhibit a marked tropism towards site of tumors. Many studies have reported that tumor progression and metastasis increase by MSCs. In contrast, other studies have shown that MSCs suppress growth of tumors. MSCs contribute to tumor growth promotion by several mechanisms: (1) transition to tumor-associated fibroblasts; (2) suppression of immune response; (3) promotion of angiogenesis; (4) stimulation of epithelial-mesenchymal transition (EMT); (5) contribution to the tumor microenvironment; (6) inhibition of tumor cell apoptosis; and (7) promotion of tumor metastasis. In contrast to the tumor-promoting properties, MSCs inhibit tumor growth by increasing inflammatory infiltration, inhibiting angiogenesis, suppressing Wnt signaling and AKT signaling, and inducing cell cycle arrest and apoptosis. In this review, we will discuss potential mechanisms by which MSC mediates tumor support or suppression and then the possible tumor-specific therapeutic strategies using MSCs as delivery vehicles, based on their homing potential to tumors.
Highlights
Mesenchymal stem cells (MSCs) are a promising source for cell therapy in regenerative medicine
MSCs can be activated by pro-inflammatory cytokines IFN-γ, TNF-α, or IL-1β [52,69,83,84,85], which are secreted by tumor cells and macrophages and produce immunomodulatory molecules, such as IDO, PGE2, IL-6, IL-10, HLA-G5, and nitric oxide (NO)
MSCs contribute to tumor growth promotion in several mechanisms, including (1) by transition to tumor associated fibroblasts; (2) by suppression of the immune response; (3) by promotion of angiogenesis; (4) by stimulation of the epithelial–mesenchymal transition (EMT); (5) through contribution to the tumor microenvironment; (6) by inhibition of tumor cell apoptosis; and (7) via promotion of tumor metastasis
Summary
Mesenchymal stem cells (MSCs) are a promising source for cell therapy in regenerative medicine. It has been shown that MSCs migrate to the tumor microenvironment and subsequently support formation of tumor vasculature, enhance the fibrovascular network, and suppress immune reactions, thereby modulating the tumor response to anti-tumor therapy (reviewed in [35,36,37,38,39]) In contrast to their tumor-promoting abilities, MSCs can suppress tumor growth via inhibition of proliferation-related signaling pathways such as AKT, PI3K, and Wnt, inhibition of cell cycle progression, downregulation of XIAP (X-linked inhibitor of apoptosis protein), and suppression of angiogenesis [40,41,42,43,44,45,46,47]. We have summarized the mechanisms of MSC-mediated effects of tumor support or suppression and discussed possible tumor-specific therapeutic strategies using MSCs as delivery vehicles, based on their homing potential to tumors
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