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Cell-derived microvesicles mediate the delivery of miR-29a/c to suppress angiogenesis in gastric carcinoma.
- Source :
-
Cancer letters [Cancer Lett] 2016 Jun 01; Vol. 375 (2), pp. 331-339. Date of Electronic Publication: 2016 Mar 18. - Publication Year :
- 2016
-
Abstract
- Microvesicles (MVs) secreted from cells have been found to mediate signal transduction between cells. In the tumor microenvironment, VEGF released from cancer cells plays a key role in promoting tumor angiogenesis. In this study, we characterized the inhibitory effect of MV-delivered miR-29a/c on angiogenesis and tumor growth in gastric cancer (GC). We found that the downregulation of miR-29a/c increases VEGF expression and release in GC cells, promoting the growth of vascular cells. By simulating the tumor microenvironment, the MV-delivered miR-29a/c significantly suppresses VEGF expression in GC cells, inhibiting vascular cell growth, metastasis, and tube formation. We also used a tumor implantation mouse model to show that secreted MVs containing overexpressed miR-29a/c significantly reduced the growth rate of the vasculature and tumors in vivo. To conclude, our results contribute to a novel anti-cancer strategy using miRNA-containing MVs to control tumor cell growth by blocking angiogenesis.<br /> (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)
- Subjects :
- Animals
Carcinoma drug therapy
Carcinoma pathology
Cell Line, Tumor
Cell Proliferation genetics
Cell-Derived Microparticles genetics
Drug Delivery Systems
Gene Expression Regulation, Neoplastic
Humans
Mice
Neovascularization, Pathologic therapy
Stomach Neoplasms drug therapy
Stomach Neoplasms pathology
Tumor Microenvironment
Vascular Endothelial Growth Factor A genetics
Xenograft Model Antitumor Assays
Carcinoma genetics
MicroRNAs genetics
Neovascularization, Pathologic genetics
Stomach Neoplasms genetics
Vascular Endothelial Growth Factor A biosynthesis
Subjects
Details
- Language :
- English
- ISSN :
- 1872-7980
- Volume :
- 375
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Cancer letters
- Publication Type :
- Academic Journal
- Accession number :
- 27000664
- Full Text :
- https://doi.org/10.1016/j.canlet.2016.03.026