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. 2016 Aug 31;74(4):697–713. doi: 10.1007/s00018-016-2346-3

Table 1.

EV interaction between cancer cells and fibroblasts

Cell types of EV donor Cell types of EV recipient EV components Functions References
Positive regulation of extracellular vesicles on cancer progression
 Cancer cells Fibroblasts TGF-β Triger the myofibroblast differentiation [19]
TGF-β Triger the myofibroblast differentiation and promote cancer growth and angiogenesis [20]
Integrins Up-regulates S100 gene expressions and promote cell growth and migration [38]
miR-155 Induce cancer-associated fibroblast-like phenotype through repressing TP53P1 [26]
miR-122 Down-regulates glucose consumption of fibroblasts [35]
 Fibroblasts Cancer cells CD81 Enhance cancer motility and metastasis [21]
Extracellular matrix proteins and ADAM10 Promote cancer motility [16]
Non-coding of transposable RNAs Expansion of therapy-resistant tumor-initiating cells [23]
miR-409 Promote epithelial-mesenchymal transition [27]
Wnt3a Expansion of cancer stem cell to enhance chemoresistance [39]
miR-21 isomiR Confer the chemo-resistance through targeting APAF1 [28]
Metabolites including amino acids and lipids Affect of metabolic properties of cancer cells [33]