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. 2019 Aug 1;9(8):1815–1829.

Table 1.

Exosome mediate the cell communication in leukemia hematopoietic microenvironment

RESOURCE RECEIVE CELL KEY MOLECULE TARGET GENE PATHWAY FUNCTION REFERENCE
AML HUVECs VEGF/VEGFR --- --- Induce glycolysis, vascular remodeling and acquisition of chemoresistance [8]
AML BMSCs --- CXCR4 Promote migration [63]
AML BMSCs --- CXCR4, c-Kit --- Promote HSPC mobilization [65]
AML --- --- BCL-2 --- Therapy resistance [71]
AML MDSCs --- --- IL-6/STAT3 signaling Immunosuppressive activity [75]
AML NK cells TGF-β1 NKG2D --- Suppressed the immune functions [77]
NB4 ECs --- --- --- Procoagulant activity [64]
drug-resistant CML sensitive CML miR-365 pro-apoptosis proteins --- Drug resistance [73]
CML ECs miR-210 Ephrin-A3 VEGF signaling Decresed angiogenesis [57]
K562 ECs pre-miR-92a integrin a5 --- Promote cell migration, tube formation [56]
K562 BMSCs --- Cxcl12, DKK1, wnt5a, IL-6 VEGF signaling Decreased production of reactive oxygen species (ROS) [59]
BCP-ALL --- IL-15 --- --- Disruption of the blood brain barrier (BBB) [66]
CLL MSCs --- -- AKT/ERK and NF-κB signaling Induce inflammatory and protumorigenic environmental conditions [67]
CLL --- miR-150, miR-155, and miR-223 --- --- Associated with a poor CLL outcome [69]
CLL NK cells --- CD16, CD56 --- Suppressed cytotoxicity [79]
APL ECs --- --- --- Increased survival [64]

Note: leukemia cell derived exosmes affected the other cells of hematopoietic microenvironment via transfor a variety of content. ‘---’ means there are no detailed informations.