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. 2019 Mar 15;51(3):29. doi: 10.1038/s12276-019-0213-7

Table 1.

Role of cancer-derived EVs in tumor progression

Biological effect Mechanism Tumor Refences
Stimulation of angiogenesis Transfer of proangiogenic mRNAs/miRNAs Renal carcinoma 11
Transfer of miR-23a and upregulation of HIF-1α Lung cancer 31
VEGF upregulation Renal carcinoma 32
Induction of c-Kit, the receptor tyrosine kinase Tie2 and Met in bone marrow progenitors Melanoma 10
Transfer of sphingomyelin, MMPs and plasminogen activator Fibrosarcoma 30
Activation of SRC signaling Chronic myeloid leukemia 33
Transfer of EDIL-3 and activation of epidermal growth factor receptor signaling Bladder cancer 35
Decrease in cell-to-cell adhesion Reduction of E-cadherin and β-catenin expression Bladder cancer 36
Downregulation of tight junction protein ZO-1 mediated by miR-23a and miR-105 Lung and breast cancer 8, 31
Increase in cell migration/invasion Transfer of KIT Gastrointestinal stromal tumor (GIST) 41
Transfer of mRNAs/miRNAs Renal carcinoma 11
Development of premetastatic niche

Recruitment and reprograming of bone marrow progenitors, inducing the transforming growth factor β secretion and upregulating fibronectin production in surrounding hepatic cells

Mediation of cancer stem cells stimulation of the premetastatic niche formation in the lungs

Pancreatic ductal adenocarcinomas (PDACs)

Renal carcinoma

42

11

Transfer of RNAs that activated Toll-like receptor 3, promoting neutrophil recruitment in the lungs Lung cancer 43
Induction of a prometastatic phenotype in bone marrow progenitors mediated by the expression of c-Kit, the receptor tyrosine kinase Tie2 and Met Melanoma 10
Immune-modulation Inhibition of dendritic cell and T-cell functions Renal and nasopharyngeal carcinoma, pancreatic, lung and breast cancer 29, 44
Promotion of tumor-supportive inflammation through the stimulation of cytokine secretion by macrophages Gastric, breast, and prostate cancer 44