TABLE 1.
EV constituents | Expression patterns | Donor/Recipient cells | Roles and mechanisms | Clinic values | Ref |
---|---|---|---|---|---|
EVs | Upregulated | HCC1806 cells/MCF10A breast cells | Strengthened the proliferation and drug resistance ability | Potential therapeutic targets | Ozawa et al. (2018) |
Exosomes ITGB4 | Overexpressing | TNBC cells/CAFs | Triggered BNIP3L-related mitochondrial autophagy and lactate production in CAFs, promote TNBC | ITGB4-induced mitophagy as targeted therapy | Sung et al. (2020) |
Exosomes | Downregulated by DET/DETD-35 | MDA-MB-231/Homologous cells | DET/DETD-35 inhibited TNBC cell activity through ROS-mediated exosomal activity and protein functions | DETD-35 as a potential anti-TNBC drug | Shiau et al. (2017) |
Exosomes miR-4516 | Upregulated | CAFs/TNBC cells | The stromal loss of miR-4516 facilitated the FOSL1-dependent proliferation and TNBC malignancy | miR-4516 as an anti-cancer drug for TNBC | Ji Eun Kim et al. (2020) |
Exosomes miR-106a-5p | Upregulated | MSCs/TNBC cells | miR-106a-5p packaged in MSC-derived exosomes promoted TNBC tumor progression in xenograft | An attractive target in TNBC treatment | Xing et al. (2021) |
Exosomes circHIF1A | Upregulated | MDA-MB-231/Homologous cells | CircHIF1A promoted TNBC growth and metastasis, and was involved in circHIF1A/NFIB/FUS positive feedback loop | A potential therapeutic target for TNBC treatment | Tong Chen et al. (2021) |
EVs cofilin-1 | Upregulated | Parent cells | Functioned as a vital regulator in EV formation and thus potentiated the formation of the pre-metastatic niche | Target cofilin-1 for the treatment of metastatic TNBC | Howard et al. (2022) |
EVs ITG β4 | Upregulated | MDA-MB-231/Homologous cells | Downregulation of ITG β4+ EVs by ARRDC3 reduced invasive potentials of TNBC EVs | Therapeutic targeting of ARRDC3/ITG β4 pathway | Soung et al. (2018) |
EVs | Upregulated | BC blood EVs/MDA-MB-231 | Induced migration and invasion via a Src-dependent pathway in TNBC | Potential therapeutic targets | Ramirez-Rícardo et al. (2020) |
Exosomes CD151 | Enriched in TNBC-derived serum exosomes | 231-CD151KO-Exo/MDA-MB-468 and MDA-MB-231 | CD151-deleted exosomes significantly decreased the migration and invasion of TNBC cells | Exosomal CD151 as a potential therapeutic target for TNBC | Sipeng Li et al. (2021) |
Exosomes UCHL1 | Upregulated | MDA-MB-436 | UCHL1 as a candidate oncoprotein that promoted TGFβ-induced BC metastasis by protecting TβRI and SMAD2 from ubiquitination | UCHL1 as a potential target for TNBC treatment | Liu et al. (2020) |
EVs SPANXB1 | Upregulated in circulating sEVs | MCF-7 cells/Homologous cells | SPANXB1 depletion prevented TNBC progression through augmented SH3GL2 expression | Potential for TNBC metastasis blocking and prognostication | Kannan et al. (2019) |
EVs IL-3R | Highly expressed in TNBC cells | TEC-EV/MDA-MB-231 cells | Anti-IL-3R-EVs and antago-miR-24-3p-EVs upregulated SPRY2 in MDA-MB-231 cells | Anti-IL-3R-EV for TNBC therapy | Lopatina et al. (2020) |
Exosomes miR-770 | Highly expressed in chemo-sensitive tissues | TNBC cells/Homologous cells | Inhibited the migration and invasion behaviors through the miR-770/STMN1 axis | A new marker for TNBC chemo-resistance and metastasis | Li et al. (2018) |
Exosomes miR-9 miR-155 | Overexpressed | MDA-MB-231 cells/MCF-7 cells | MiR-9 and miR-155 were enriched in metastatic BC exosomes targeting PTEN and DUSP14 | Novel therapy methods for TNBC metastasis | kia et al. (2019) |
MVs miR-221 | Overexpressed | MDA-MB-231 cells/Homologous cells | Promoted EMT and metastasis phenotypes in a PTEN/AKT/NF-ĸB/miR221 dependent manner | A potential therapeutic approach for tumorigenesis and metastasis | Das et al. (2019) |
Exosomes miR-939 | Upregulated | MDA-MB-231 cells/endothelial cells | Downregulated VE-cadherin and destroyed the barrier function of endothelial monolayers | A potential therapeutic target for TNBC invasion | Di Modica et al. (2017) |
Exosomes circPSMA1 | Overexpressed | TNBC cell lines/Homologous cells | Promoted tumorigenesis, metastasis, and immunosuppression state by regulating the circPSMA1/miR-637/Akt axis | A potential target for TNBC treatment | Su-jin Yang et al. (2021) |
CAFs, cancer-associated fibroblast; DET, deoxyelephantopin; DETD-35, DET derivative-35; EMT, epithelial to mesenchymal transition; EVs, extracellular vesicles; ITGB4, integrin beta 4; MSCs, mesenchymal stem cells; ROS, reactive oxygen species; TNBC, triple-negative breast cancer; TEC, tumor-endothelial cells.