The mechanisms of mutual relationship between malignant hematologic cells and mesenchymal stem cells: Does it contradict the nursing role of mesenchymal stem cells?

Table 1 Communication between MSCs and hematologic malignancies/cell lines through tunneling nanotubes (TNTs) and its effects

Type of malignancy/cell	Kind of material transferred	Target	Results	References
ALL	Pro-survival cytokines	ALL cells	Conversion to a leukemia pro-survival	[35]
ALL	IL-6/TNFα/IL-1β	ETV6‐RUNX1 harboring cells	DNA damage accumulation	[48]
BCP-ALL	Autophagosomes, mitochondria, ICAM1 and other lipophiles	MSCs	Cytokine secretion, leukemic cell survival, drug resistance	[34]
Jurkat cells	Mitochondria	Mostly MSCs	Leukemic cell survival, ↓ROS, chemoresistance	[36, 37] [38]
AML	Mitochondria	AML cells	Chemoresistance, cytotoxic effects of the nucleoside analog ARA-C	[39]
AML	Autophagosome	AML cells	Autophagy	[32]
AML	NADPH oxidase 2 (NOX2) superoxide	MSCs	Enhances transferring from MSC to AML	[41]
CML	Cellular vesicles	Bi-directional	Imatinib resistance, ↓imatinib mediated caspase activity, apoptosis	[44]
Multiple myeloma	NADPH oxidase 2 (NOX2) superoxide	MM cell	Enhances transferring from MSC to MM cells	[41]
B-cell lymphoma	Mitochondria, soluble factors	MSCs	Anti-apoptosis: upregulate BCL-2 family proteins Pro-oncogenic: Activation of NOTCH1 signaling	[46]
MDS	Proangiogenic factors (VEGF-A, IGFs, and EGFs) and mediators of fibrosis (LOXL, TGF-β, and LIF)	Bi-directional	MSCs adopt MDS-desirable features, Mitochondria dysfunction, genotoxic stress in HSCs, ↑ risk of developing to AML, Impaired myeloid and lymphoid differentiation in mice with MDS, Modulated expression of several cytokines in MSCs	[49]

ISSN: 1478-811X