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Table 1 Some representative contents of EVs, their functions and mechanism

From: Role of extracellular vesicles in tumour microenvironment

Disease EV Contents Pathways/Mechanism Function
Glioma EGFRvIII MAPK, Akt tumour development
LncRNA-HOTAIR upregulating VEGF-A expression angiogenesis
Glioblastoma VEGF-A vascular leakiness, angiogenesis
Melanoma Met resistance lung metastasis
PDGFR-β PI3K/AKT resistance
upregulation of S100a8, S100a9, and TNF-α vascular leakiness
miR-191 and let-7a EMT
PD-L1 competitive inhibition Anti-PD-1 therapy resistance
HCC HGF HGF/c-MET/PI3K/AKT resistance
LncRNA-ROR TGF-β resistance
Osteosarcoma P-gp/MDR-1 mRNA resistance
TGF-β secreting IL-6 tumour metastasis
RCC Lnc-ARSR STAT3, AKT, ERK resistance
Breast cancer LncRNA-UCA1 resistance
upregulating a subset of S100 proteins and triggering Src kinase signalling vascular leakiness
miR-23a, miR-105 targeting ZO-1 vascular leakiness
miR-9 shift of normal FBs into tFBs
HER2 competitive inhibition Trastuzumab resistance
PDAC circ-PDE8A miR-338/MACC1/MET tumour invasion
Lung cancer miR-23a, miR-105 targeting ZO-1 vascular leakiness
Myeloma syndecan-1, VEGF, HGF angiogenesis
EGFR MAPK, AKT angiogenesis
UBC LncRNA-HOTAIR EMT
circPRMT5 miR-30c “sponge” EMT
Gastric cancer LncRNA-ZFAS1 EMT
Pancreatic cancer SELPLG coagulation and metastasis
HNSCC PD-L1 competitive inhibition immunosuppression, tumour progression
Prostate cancer PD-L1 competitive inhibition immunosuppression
B-cell lymphoma CD20 competitive inhibition rituximab resistance