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Exosomal transfer of miR-126 promotes the anti-tumour response in malignant mesothelioma: Role of miR-126 in cancer-stroma communication
F. Monaco, S. Gaetani, F. Alessandrini, A. Tagliabracci, M. Bracci, M. Valentino, J. Neuzil, M. Amati, M. Bovenzi, M. Tomasetti, L. Santarelli,
Language English Country Ireland
Document type Journal Article
Grant support
NV16-31604A
MZ0
CEP Register
- MeSH
- EGF Family of Proteins metabolism MeSH
- Exosomes metabolism MeSH
- Fibroblasts metabolism MeSH
- Carcinogenesis metabolism MeSH
- Cells, Cultured MeSH
- Humans MeSH
- Cell Communication physiology MeSH
- Mesothelioma metabolism MeSH
- MicroRNAs metabolism MeSH
- Lung Neoplasms metabolism MeSH
- Calcium-Binding Proteins metabolism MeSH
- Signal Transduction physiology MeSH
- Vascular Endothelial Growth Factor A metabolism MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
MiR-126 has been shown to suppress malignant mesothelioma (MM) by targeting cancer-related genes without inducing toxicity or histopathological changes. Exosomes provide the opportunity to deliver therapeutic cargo to cancer stroma. Here, a tumour stromal model composed of endothelial cells (HUVECs), fibroblasts (IMR-90 cells), non-malignant mesothelial cells (Met-5A cells) and MM cells (H28 and MM-B1 cells) was used. The cells were treated with exosomes from HUVECs carrying endogenous (exo-HUVEC) and enriched miR-126 (exo-HUVECmiR-126), and the uptake/turnover of exosomes; miR-126 distribution within the stroma; and effect of miR-126 on cell signalling, angiogenesis and cell proliferation were evaluated. Based on the sensitivity of MM cells to exo-HUVEC miR-126 treatment, miR-126 was distributed differently across stromal cells. The reduced miR-126 content in fibroblasts in favour of endothelial cells reduced angiogenesis and suppressed cell growth in an miR-126-sensitive environment. Conversely, the accumulation of miR-126 in fibroblasts and the reduced level of miR-126 in endothelial cells induced tube formation in an miR-126-resistant environment via VEGF/EGFL7 upregulation and IRS1-mediated cell proliferation. These findings suggest that transfer of miR-126 via HUVEC-derived exosomes represents a novel strategy to inhibit angiogenesis and cell growth in MM.
References provided by Crossref.org
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- $a Monaco, Federica $u Department of Clinical and Molecular Sciences, Section of Experimental and Occupational Medicine, Polytechnic University of Marche, Via Tronto 10/A, 60126, Ancona, Italy.
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- $a MiR-126 has been shown to suppress malignant mesothelioma (MM) by targeting cancer-related genes without inducing toxicity or histopathological changes. Exosomes provide the opportunity to deliver therapeutic cargo to cancer stroma. Here, a tumour stromal model composed of endothelial cells (HUVECs), fibroblasts (IMR-90 cells), non-malignant mesothelial cells (Met-5A cells) and MM cells (H28 and MM-B1 cells) was used. The cells were treated with exosomes from HUVECs carrying endogenous (exo-HUVEC) and enriched miR-126 (exo-HUVECmiR-126), and the uptake/turnover of exosomes; miR-126 distribution within the stroma; and effect of miR-126 on cell signalling, angiogenesis and cell proliferation were evaluated. Based on the sensitivity of MM cells to exo-HUVEC miR-126 treatment, miR-126 was distributed differently across stromal cells. The reduced miR-126 content in fibroblasts in favour of endothelial cells reduced angiogenesis and suppressed cell growth in an miR-126-sensitive environment. Conversely, the accumulation of miR-126 in fibroblasts and the reduced level of miR-126 in endothelial cells induced tube formation in an miR-126-resistant environment via VEGF/EGFL7 upregulation and IRS1-mediated cell proliferation. These findings suggest that transfer of miR-126 via HUVEC-derived exosomes represents a novel strategy to inhibit angiogenesis and cell growth in MM.
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