Table 1.
Role that some bioactive molecules play in cancer evolution as exosomal cargo.
| Exosomal Cargo | Biological Function | Cancer Type | Ref. | ||
|---|---|---|---|---|---|
| Bioactive Molecule | Type | Mechanism | |||
| Delta-like | Protein | Notch signal inhibition | Increased angiogenesis | Tumour xenograft model | [142] |
| EGFR VIII | Protein | Promotes Akt and MAPK pathways | Increased anchorage-independent growth | Glioma | [64] |
| Integrins | Protein | Induce src and up-regulate proinflammatory s-100 genes |
Leading exosomes to specific tissues | Breast | [130] |
| MET | Protein | Promotes MET signal | Increased prometastatic activity of bone marrow cells | Melanoma | [129] |
| MIF | Protein | Promotes TGF-beta signal-induced fibronectin production | Favoured premetastatic niche formation at liver | Pancreatic | [68] |
| TGF-beta | Protein | Promotes SMAD-related signal Induces mesenchymal stem cell differentiation into myofibroblasts |
Induced fibroblast FGF2 production, increased cancer proliferation and invasiveness |
Prostate | [65,122] |
| CD63, CD81, HSP90, HSP70, TNF1-alpha, MMP2, MMP9, annexin-II | Proteins | Increase TGF-beta 2, TNF1-alpha, IL-6, TSG101, Akt, ILK1, beta-catenin signalling; remodelling of epithelial adherent junctions | Increased stemness, metastasis and CAFs formation | Prostate | [143] |
| Fasl, TGF-beta, galectin-9, HSP72 | Proteins | Transfer of Fasl, TGF-beta, NKG2D ligands, galectin-9, HSP72 into immune cells | Evasion of immune responses | - | [79,80,81,82,83,84] |
| Integrin av-beta3 | Protein | Promotes cell migration on its ligand, vitronectin | Promotion of a migratory phenotype | Prostate | [144] |
| PD-L1 | Protein | PD-L1 up-regulation | Immune checkpoint regulator | Melanoma | [145] |
| Tspan8 | Protein | Selective recruitment of proteins and mRNA | Induces endothelial cell proliferation, migration and sprouting | Rat adenocarcinoma model | [17] |
| miR-9 | miRNA | Modulation of genes involved in cell motility and extracellular matrix remodelling pathways | CAF-like induction | Breast | [121] |
| miR-21 | miRNA | Regulates PTEN/PI3K/AKT signal | Apoptosis inhibition | Gastric | [125] |
| miR-105 | miRNA | Down-regulates tight junctions | Vascular endothelial barrier destruction | Breast | [139] |
| miR-181c | miRNA | Down-regulates PDPK1/cofilin signal | Blood-brain barrier destruction | Breast | [140] |
| miR-200 | miRNA | Regulates gene expression and EMT | Induction of cancer metastatization to the lung | Breast | [136] |
| miR-222-3p | miRNA | Regulates SOCS3/STAT3 pathway | Induction of TAM polarization | Epithelial ovarian | [85] |
| ZFAS1 | lncRNA | Governs MAPK signal and EMT transcription factors | Induction of cell cycle progression and EMT | Gastric | [59] |
| hTERT mRNA | mRNA | Converts nonmalignant fibroblast into telomerase positive cells | Phenotypic changes (increased proliferation and extension of life span) |
Pancreatic and lung | [67] |
| TCA-cycle intermediate | Metabolite | Governs mitochondrial oxidative phosphorylation, glycolysis, glutamine-dependent reductive carboxylation | Down-regulation of mitochondrial function and up-regulation of glucose metabolism | Prostate | [66] |
EGFR: epidermal growth factor; Akt: protein kinase B; MAPK: mitogen-activated protein kinase; MIF: migration inhibitor factor; TGF: tumour growth factor; FGF: fibroblast growth factor; HSP: heat shock protein; TNF: tumour necrosis factor; MMP: matrix metalloproteinase; IL: interleukin; ILK: integrin-linked kinase; CAFs: cancer-associated fibroblasts; Fasl: Fas ligand; NKG2D: natural killer group 2D; PD-L1: programmed death-ligand 1; Tspan8: tetraspanin-8; miR: micro RNA; PTEN: phosphatase and tensin homolog; PI3K: phosphoinositide 3-kinase; PDPK1: 3-phosphoinositide-dependent protein kinase 1; EMT: epithelial to mesenchymal transition; SOCs: suppressor of cytokine signalling proteins; STAT: signal transducer and activator of transcription 3; TAMs: tumour associated macrophages; hTERT: human telomerase reverse transcriptase; TCA cycle: tricarboxylic acid cycle (Krebs’ cycle).