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Table 1 TME promotes the formation and release of TEXs

From: Tumor-derived exosomes, myeloid-derived suppressor cells, and tumor microenvironment


Type of cancer



Extracellular acidity


Human metastatic melanoma cells release more exosomes under an acidic condition. Ganglioside GM3 and caveolin-1 are enriched in TEXs released at low pH.


Prostate cancer

Acidity of TME facilitates the release of TEXs expressing PSA and CD81. Extracellular acidity leads to the spill-over of TEXs into the peripheral blood of patients with prostate cancer.



Lung cancer

Lung cancer cells produce more miR-23a-contained exosomes under hypoxic condition. Exosomal miR-23a can enhance the angiogenesis, vascular permeability, and transendothelial migration of lung cancer.


Ovarian cancer

Hypoxia significantly increases the release of TEXs in ovarian cancer by reducing endolysosomal fusion and increasing the expression of TFEB. Additionally, hypoxic conditions induce the upregulation of Rab27a and downregulation of Rab7 by activating STAT3 to promote the release of TEXs.


Bladder cancer

LncRNA-UCA1 is enriched in hypoxic bladder cancer cell-derived TEXs, and hypoxic exosomal lncRNA-UCA1 can promote tumor growth and progression though accelerating EMT.


Genotoxic stress

Multiple myeloma

Genotoxic stress facilitates the release of exosomes from MM cells. MM cell-derived exosomes are able to promote IFN-γ production of NK cells in TME by activating NF-κB pathway in a TLR2/Hsp70-dependent manner.



Lung cancer

Phosphorylated PKM2 form a dimer structure with low pyruvate kinase activity but high protein kinase activity. It then associates with SNAP-23 near cells' membranes, leading to SNAP-23 phosphorylation at Ser95 and upregulation of TEXs release

[94, 95]

Rab27A Rab27B

Bladder cancer

/Cervical cancer

/Breast cancer /Melanoma

/Lung adenocarcinoma

Rab27A regulates docking and membrane fusion of MVEs, whereas Rab27B participates in the transfer of membranes from the TGN to MVEs. Rab27A/B-induced exosome secretion decreases the expression of tumor-suppressive microRNAs.

[96, 97]


Lung cancer

TSAP6 and maspin induced by p53 play a key role in the exosome-mediated secretion. The secreted proteins may be involved in cell-cell communication.


Colorectal cancer

Knockdown of TP53 which is encoding gene of p53 protein induces colorectal cancer cells to produce exosomes with reduced sizes in a HGS-dependent manner.


Gastric cancer

p53−/− MSC exosomes deliver UBR2 to target cells and promote gastric cancer growth and metastasis by regulating Wnt/β-catenin pathway.




EGFRvIII changes the expressing profile of exosome-associated proteins and their protein compositions in GBM. TEXs from EGFRvIII expressing glioma cells are enriched with focal adhesion related proteins to promote the invasion of cancer cells.



Lyeloma/lymphoblastoid/breast cancer

Heparanase drives exosome secretion, alters exosome composition, and facilitates production of exosomes that impact both tumor and host cell behavior.


Mammary ductal carcinoma

Heparanase promotes endosomal membrane budding and modulates the biogenesis of exosomes by activating the syndecan-syntenin-ALIX pathway.

[103, 104]


Lung cancer

C-terminal fragment of Dsg2 enhances the release of TEXs and promotes the package of EGFR and c-Src into TEXs.


  1. Lists the tumor microenvironmental conditions discussed in this review which are capable of contributing to the formation and release of TEXs