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. 2015 Apr 1:3:23.
doi: 10.3389/fcell.2015.00023. eCollection 2015.

Cancer-associated mesenchymal stem cells aggravate tumor progression

Chie Kudo-Saito  1
Affiliations

Cancer-associated mesenchymal stem cells aggravate tumor progression

Chie Kudo-Saito. Front Cell Dev Biol. .

Abstract

Mesenchymal stem cells (MSCs) have both stemness and multi-modulatory activities on other cells, and the immunosuppressive and tumor-promotive mechanisms have been intensively investigated in cancer. The role of MSCs appears to be revealed in tumor aggravation, and targeting MSCs seems to be a promising strategy for treating cancer patients. However, it is still impractical in clinical therapy, since the precise MSCs are poorly understood in the in vivo setting. In previous studies, MSCs were obtained from different sources, and were prepared by ex vivo expansion for a long term. The inconsistent experimental conditions made the in vivo MSCs obscure. To define the MSCs in the host is a priority issue for targeting MSCs in cancer therapy. We recently identified a unique subpopulation of MSCs increasing in mice and human with cancer metastasis. These MSCs are specifically expanded by metastatic tumor cells, and promote tumor progression and dissemination accompanied by immune suppression and dysfunction in the host, more powerfully than normal MSCs growing without interference of cancer. In this review, we summarize current knowledge of the role of MSCs in tumor aggravation, along with our new findings of the bizarre MSCs.

Keywords: cancer; epithelial-to-mesenchymal transition; immunosuppression; mesenchymal stem cell; metastasis.

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Figures

Figure 1
Figure 1
Tumor aggravation caused by the sMSCs. When EMT happens in tumor cells, the Snail+ metastatic tumor cells generate and expand multifunctional sMSCs that highly release FSTL1, CCL2, CCL3, and ANGPT2 for potentiating tumor aggravation. The sMSCs promote tumor progression and metastasis by building tumor heterogeneity within the microenvironment, and induce immune suppression and dysfunction for further accelerating the tumor survival and escape.
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