Skip to main content

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