The Activation of Mesenchymal Stem Cells by Glioblastoma Microvesicles Alters Their Exosomal Secretion of miR-100-5p, miR-9-5p and let-7d-5p

Garnier, Delphine; Ratcliffe, Edward; Briand, Joséphine; Cartron, Pierre-François; Oliver, Lisa; Vallette, François M.

doi:10.3390/biomedicines10010112

Cited by 16 publications

(12 citation statements)

References 72 publications

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“…For example, in the work of Guillén et al the size of EVs from adipose tissue-derived MSC was analyzed and the average vesicle diameter was 295 nm for MVs and 115 nm for exosomes [ 20 ]. Similar results were reported by Garnier et al where EVs from glioblastoma were separated using differential centrifugation [ 21 ]. In another work, it was shown that MVs can have a size from 500 to 1500 nm [ 22 ].…”

Section: Discussionsupporting

confidence: 88%

Comparative Analysis of Natural and Cytochalasin B-Induced Membrane Vesicles from Tumor Cells and Mesenchymal Stem Cells

Gilazieva

Chulpanova

Ponomarev

et al. 2022

CIMB

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To date, there are numerous protocols for the isolation of extracellular vesicles (EVs). Depending on the isolation method, it is possible to obtain vesicles with different characteristics, enriched with specific groups of proteins, DNA and RNA, which affect similar types of cells in the opposite way. Therefore, it is important to study and compare methods of vesicle isolation. Moreover, the differences between the EVs derived from tumor and mesenchymal stem cells are still poorly understood. This article compares EVs from human glioblastoma cells and mesenchymal stem cells (MSCs) obtained by two different methods, ultracentrifugation and cytochalasin B-mediated induction. The size of the vesicles, the presence of the main EV markers, the presence of nuclear and mitochondrial components, and the molecular composition of the vesicles were determined. It has been shown that EVs obtained by both ultracentrifugation and cytochalasin B treatment have similar features, contain particles of endogenous and membrane origin and can interact with monolayer cultures of tumor cells.

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Section: Discussionsupporting

confidence: 88%

Comparative Analysis of Natural and Cytochalasin B-Induced Membrane Vesicles from Tumor Cells and Mesenchymal Stem Cells

Gilazieva

Chulpanova

Ponomarev

et al. 2022

CIMB

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“…It is likely that GSCs can modulate the tumour microenvironment and nearby non-GSC cells into a more proliferative or migratory phenotype by releasing EVs with specific cargo contents. This is evident in studies where GSC-EVs can modulate the activity of mesenchymal stem cells and their miRNA profiles, by mechanisms such as decreasing anti-tumour miRNAs [ 48 ] or transferring EGFRvIII molecules to cause a cellular transformation of recipient cells [ 41 ], or where EVs release the invasiveness-related proteins into the microenvironment to degrade the extracellular matrix [ 49 ]. Our data are also in agreement with a recent study by Pan et al [ 44 ], demonstrating that glioblastoma-derived EVs can promote proliferation, migration and intercellular communication in surrounding tumour cells by manipulating the PI3K-Akt-mTOR pathway.…”

Section: Discussionmentioning

confidence: 99%

Extracellular Vesicles Secreted by Glioma Stem Cells Are Involved in Radiation Resistance and Glioma Progression

Nguyen

Jones

et al. 2022

IJMS

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Glioblastoma is the most aggressive brain tumour with short survival, partly due to resistance to conventional therapy. Glioma stem cells (GSC) are likely to be involved in treatment resistance, by releasing extracellular vesicles (EVs) containing specific molecular cargoes. Here, we studied the EVs secreted by glioma stem cells (GSC-EVs) and their effects on radiation resistance and glioma progression. EVs were isolated from 3 GSCs by serial centrifugation. NanoSight measurement, cryo-electron microscopy and live imaging were used to study the EVs size, morphology and uptake, respectively. The non-GSC glioma cell lines LN229 and U118 were utilised as a recipient cell model. Wound healing assays were performed to detect cell migration. Colony formation, cell viability and invadopodium assays were conducted to detect cell survival of irradiated recipient cells and cell invasion post GSC-EV treatment. NanoString miRNA global profiling was used to select for the GSC-EVs’ specific miRNAs. All three GSC cell lines secreted different amounts of EVs, and all expressed consistent levels of CD9 but different level of Alix, TSG101 and CD81. EVs were taken up by both LN229 and U118 recipient cells. In the presence of GSC-EVs, these recipient cells survived radiation exposure and initiated colony formation. After GSC-EVs exposure, LN229 and U118 cells exhibited an invasive phenotype, as indicated by an increase in cell migration. We also identified 25 highly expressed miRNAs in the GSC-EVs examined, and 8 of these miRNAs can target PTEN. It is likely that GSC-EVs and their specific miRNAs induced the phenotypic changes in the recipient cells due to the activation of the PTEN/Akt pathway. This study demonstrated that GSC-EVs have the potential to induce radiation resistance and modulate the tumour microenvironment to promote glioma progression. Future therapeutic studies should be designed to interfere with these GSC-EVs and their specific miRNAs.

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“… 25 , 26 Angus J loaded doxorubicin into MSC-EXO using electroporation to reduce metabolic degradation and demonstrated increased accumulation in tumor tissue compared with free doxorubicin. 27 Furthermore, recognition of MSC-EXO membrane receptors by tumor cells may facilitate passive ingestion of cytocidal drugs. 28 , 29 In addition, tumor targeting may be enhanced by engineering of folate receptors into EXO.…”

Section: Discussionmentioning

confidence: 99%

Activation of Dynamin-Related Protein 1 and Induction of Mitochondrial Apoptosis by Exosome-Rifampicin Nanoparticles Exerts Anti-Osteosarcoma Effect

Chen¹,

Lin²,

Yu³

et al. 2022

IJN

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Purpose To investigate induction of cell death in Osteosarcoma (OS) using the anti-tuberculosis drug, rifampicin, loaded into exosomes. Patients and Methods BMSC-exosomes were isolated by ultracentrifugation and loaded ultrasonically with rifampicin. Nanoparticle exosome-rifampicin (EXO-RIF) was added to the OS cell-lines, 143B and MG63, in vitro, to observe the growth inhibitory effect. In vivo experiments were conducted by injecting fluorescently labeled EXO-RIF through the tail vein of 143B cell xenograft nude mice and tracking distribution. Therapeutic and toxic side-effects were analyzed systemically. Results Sonication resulted in encapsulation of rifampicin into exosomes. Exosome treatment accelerated the entry of rifampicin into OS cells and enhanced the actions of rifampicin in inhibiting OS proliferation, migration and invasion. Cell cycle arrest at the G2/M phase was observed. Dynamin-related protein 1 (Drp1) was activated by EXO-RIF and caused mitochondrial lysis and apoptosis. Exosome treatment targeted rifampicin to the site of OS, causing OS apoptosis and improving mouse survival in vivo. Conclusion The potent Drp1 agonist, rifampicin, induced OS apoptosis and exosome loading, improving OS targeting and mouse survival rates. EXO-RIF is a promising strategy for the treatment of diverse malignancies.

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The Activation of Mesenchymal Stem Cells by Glioblastoma Microvesicles Alters Their Exosomal Secretion of miR-100-5p, miR-9-5p and let-7d-5p

Cited by 16 publications

References 72 publications

Comparative Analysis of Natural and Cytochalasin B-Induced Membrane Vesicles from Tumor Cells and Mesenchymal Stem Cells

Comparative Analysis of Natural and Cytochalasin B-Induced Membrane Vesicles from Tumor Cells and Mesenchymal Stem Cells

Extracellular Vesicles Secreted by Glioma Stem Cells Are Involved in Radiation Resistance and Glioma Progression

Activation of Dynamin-Related Protein 1 and Induction of Mitochondrial Apoptosis by Exosome-Rifampicin Nanoparticles Exerts Anti-Osteosarcoma Effect

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