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Endothelial‐derived Extracellular Vesicles Induce Proliferation in Glioblastoma Cells
Author(s) -
Zimmerman Zachary R.,
Dores Michael Robert
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.804.55
Subject(s) - microvesicles , microbiology and biotechnology , extracellular , endothelium , endothelial stem cell , biology , cell growth , exosome , angiogenesis , cd63 , intracellular , cancer research , biochemistry , endocrinology , in vitro , microrna , gene
Extracellular vesicles (ECVs) are critical biomarkers for disease and mediate intracellular signaling within the tumor microenvironment. ECVs from tumors enhance cell proliferation and migration in endothelial cells. However, the role of endothelial ECVs in regulating tumor cell proliferation is not well understood. We have investigated the role ECVs play in the communication between glioblastoma cancers and the human endothelium. To determine the effect of ECVs on the communication between glioblastoma multiforme cancer and endothelial cells, ECVs from both cell types were isolated. These ECVs were determined to carry the proteins CD63 and ALIX, known exosome biomarkers and proteins found in extracellular vesicles originating from the multivesicular body. Glioblastoma cells treated with ALIX‐positive exosomes collected from endothelial cells demonstrate increased migration over untreated cells. Signaling through G protein‐coupled receptors modulates ECV content in endothelial exosomes and increases the amount of ALIX‐positive ECVs released. We are investigating whether changing ECV content through GPCR signaling increases their ability to induce proliferation in glioblastoma cells. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .