Abstract
Mesenchymal stem cells (MSCs) are known for being multi-potent. However, they also possess anticancer properties, which has prompted efforts to adapt MSCs for anticancer therapies. However, MSCs have also been widely implicated in pathways that contribute to tumor growth. Numerous studies have been conducted to adapt MSCs for further clinical use; however, the results have been inconclusive, possibly due to the heterogeneity of MSC populations. Moreover, the conflicting roles of MSCs in tumor inhibition and tumor growth impede their adaptation for anticancer therapies. Antitumorigenic and protumorigenic properties of MSCs in hematologic malignancies are not as well established as they are for solid malignancies, and data comparing them are still limited. Herein the effect of MSCs on hematologic malignancies, such as leukemia and lymphoma, their mechanisms, sources of MSCs, and their effects on different types of cancer, have been discussed. This review describes how MSCs preserve both antitumorigenic and protumorigenic effects, as they tend to not only inhibit tumor growth by suppressing tumor cell proliferation but also promote tumor growth by suppressing tumor cell apoptosis. Thus clinical studies trying to adapt MSCs for anticancer therapies should consider that MSCs could actually promote hematologic cancer progression. It is necessary to take extreme care while developing MSC-based cell therapies in order to boost anticancer properties while eliminating tumor-favoring effects. This review emphasizes that research on the therapeutic applications of MSCs must consider that they exert both antitumorigenic and protumorigenic effects on hematologic malignancies.
Highlights
Since the identification of mesenchymal stem cells (MSCs) from adult bone marrow (BM) [1], numerous studies haveThese authors contributed : Myoung Woo Lee, Somi RyuUniversity School of Medicine, Jinju, Korea 5 Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, Korea been performed globally to understand their characteristics and functions
The failure of MSCs to be adapted into anticancer therapies is usually due to recurrence or relapse after the therapy, rather than a lack of primary response or initial remission [80]
MSCs have been shown to promote mammosphere formation partially via the epidermal growth factor (EGF)/EGF receptor/Akt pathway to regulate self-renewal through cytokine networks in breast cancer cells [132, 133]. They regulate cancer stem cells via bone morphogenic protein signaling in ovarian cancer [134] and provide favorable tumor-promoting microenvironments through WNT/transforming growth factor (TGF)-β signaling pathways in gastric carcinoma [135]. Besides their role in solid cancers, MSCs increase the stemness of cells in hematologic malignancies such as multiple myeloma via an activation of the Bruton tyrosine kinase signal pathway [136]
Summary
Since the identification of mesenchymal stem cells (MSCs) from adult bone marrow (BM) [1], numerous studies have. Further research is needed to study the mechanisms of tumor cell cycle arrest that lead to the antitumor effects of MSCs on hematologic malignancies. MSCs have been shown to promote mammosphere formation partially via the epidermal growth factor (EGF)/EGF receptor/Akt pathway to regulate self-renewal through cytokine networks in breast cancer cells [132, 133] They regulate cancer stem cells via bone morphogenic protein signaling in ovarian cancer [134] and provide favorable tumor-promoting microenvironments through WNT/TGF-β signaling pathways in gastric carcinoma [135]. Besides their role in solid cancers, MSCs increase the stemness of cells in hematologic malignancies such as multiple myeloma via an activation of the Bruton tyrosine kinase signal pathway [136]. They suggested different underlying mechanisms involving Notch signaling driven by Notch receptors, because significant upregulation of Jagged and overexpression of Notch were observed when Jurkat cells and UC-MSCs were co-cultured
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