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Table 2 Role of exosomal proteins in glioma

From: Role of exosomes in malignant glioma: microRNAs and proteins in pathogenesis and diagnosis

Exosomal protein

Expression status

Target

Note

Ref

HMGB1

Up

SASH1

HMGB1 plays different roles depending on its location: as an extracellular protein, HMGB1 decreases SASH1 expression, but as an exosomal protein, HMGB1 increases SASH1 expression

[140]

IL-8, PDGFs, caveolin 1, and lysyl oxidase

Up

–

The exosomal pathway constitutes a potential target that drives hypoxia-dependent intercellular signaling during tumor development.

[141]

L1CAM

Up

FGFR, FAK

Increases cell motility, proliferation, and invasiveness.

[142]

STC1, STC2

Up

–

Induces cell migration in a hypoxia-dependent manner

[143]

EGFRvIII

Up

CD44, BSG, CD151, CD81 and CD82

–

[144]

VEGF-A

Up

claudin-5 and occluding

Increases the permeability of the BBB in vitro by interrupting the expression of claudin-5 and occludin.

In vivo permeability assay showed hypoxic GBM-derived exosomes remained functional in the blood circulation and induced permeability in the BBB.

[145]

CRYAB

Up

–

The U373 glioma cells produce and secrete cryAB in exosomes; stimulation with IL-1β and TNF-α significantly increased the levels of cryAB not only in cells but also in secreted exosomes.

[146]

PTRF

Up

Cavin1

PTRF over-expression increases exosome secretion and induces cell growth in vitro.

Clinical samples showed a positive correlation between tumor grade and PTRF expression in both tumor tissue and exosomes isolated from blood harvested from glioma patients.

[147]

PD-1

Up

–

–

[148]

IL-8, ZAP70, TGF-β

down

ELISPOT, IL-13R,

–

[148]

IL13Rα2, IL13QD

Up

–

Specific binding of IL13QD to tumor associated exosomes was confirmed.

[149]

CAV1

Up

p-ERK1/2

Exosome uptake appears to be dependent on intact ERK1/2-HSP27 signaling, and ERK1/2 phosphorylation was negatively influenced by CAV1 during internalization of exosomes.

[150]

NK-Exo

Up

CD63, Alix

In vivo NK-Exo treatment inhibited tumor xenograft growth compared to control mice, and pretreatment of mice with dextran sulfate 2 h before NK-Exo treatment increased the antitumor effect of NK-Exo compared to control and NK-Exo-alone-treated mice.

[151]

SRSF1, SRSF3

Up

PTBP1,PTBP2

–

[152]

NANOGP8

Up

–

–

[153]

IFN-gamma, granzyme B

Down

–

Granzyme B was significantly inhibited in CD8 + T cells exposed to GL26 cell-derived exosomes, and the exosomes could not inhibit the expression of granzyme B in CD4 + T cells and NK cells.

[154]

PTENP1

Up

miR-10a-5p

The lncRNA PTENP1 could be packaged into exosomes from hUC-MSCs, transferred to U87 cells, and then stabilized PTEN by competitively binding miR-10a-5p.

[155]

CLIC1

Up

GFP, FLAG-tagged

CLIC1 is a circulating protein, secreted via extracellular vehicles (Evs) released by either cell lines or GBM-derived CSCs.

[156]

K-Ras

Up

Raf-RBD

–

[157]

immunoglobulin (Ig) G2 and IgG4

Up

CD163

–

[158]

TrkB

Up

YKL-40

Inhibits tumor growth in vivo.

Plays a key role in the control of GBM progression and aggressiveness.

[159]

MGMT mRNA

Up

–

–

[160]

EGFRvIII

Up

CD81

EGFRvIII expression either in exosomes or tissue was correlated with poor survival.

[161]

N-glycoproteins

Up

Glycopeptide

329 N-glycosylation sites corresponding to 180 different N-glycoproteins were enriched and identified in plasma exosomes of glioma patients and healthy subjects.

[162]

LOX, ADAMTS1, TSP1, VEGF

Up

KCNJ3

Induces differential gene expression in recipient glioma cells

[163]

CRCL

Down

T cell

Anti-tumor activity through modulating Cbl-b and c-Cbl signaling.

[164]

NF-κB

Up

green fluorescent protein

NF-κB inducible promoter mediates widespread reporter gene expression in tumor-associated myeloid-derived cells after systemic injection of exo-AAV in brain tumor-bearing mice

[165]

Glut-1, HK-2, and PKM-2

Up

MMP-2, MMP-9

Increases glucose consumption and generation of lactate and ATP.

[166]

TDP-43

Up

–

–

[167]