TMIC-09GLIOBLASTOMA STEM CELL-DERIVED EXOSOMES PROMOTE M2 POLARIZATION OF HUMAN MONOCYTES (original) (raw)
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The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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Jun Wei ,
The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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Xu Li ,
The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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John Yu ,
The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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The University of Texas MD Anderson Cancer Center, Houston, TX, USA
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Published:
09 November 2015
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Konrad Gabrusiewicz, Yuuri Hashimoto, Jun Wei, Maiti Sourindra, David Hawke, Xu Li, Shouhao Zhou, John Yu, Shinji Yamashita, Joy Gumin, Anna Zal, Felix Nwajei, Tomasz Zal, Frederick Lang, Laurence Cooper, Amy Heimberger, TMIC-09
GLIOBLASTOMA STEM CELL-DERIVED EXOSOMES PROMOTE M2 POLARIZATION OF HUMAN MONOCYTES, Neuro-Oncology, Volume 17, Issue suppl_5, November 2015, Page v216, https://doi.org/10.1093/neuonc/nov236.09
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INTRODUCTION: Exosomes secreted by cancer cells have pleiotropic functions, and can promote autocrine signaling to distant cells. Elucidating the mechanistic modulation of the immune system by these exosomes provides insight into potential biomarkers for detection, recurrence, and response, and identifies potential new therapeutic targets. METHODS: Exosomes were isolated from human glioblastoma stem cells (GSC) and fibroblasts (control) using differential centrifugation. Fluorescent-labeled exosomes were co-cultured with human peripheral blood mononuclear cells (PBMCs). Flow cytometry and confocal microscopy methods were utilized to determine the ability of immune cells to uptake exosomes and to evaluate subsequent intracellular trafficking. The exosomal protein and RNA content was analyzed by mass spectrometry and Nanostring Counter System, respectively. The phenotypic and functional skewing of the monocyte lineage was analyzed after exposing these cells to exosomes. The cytokine array was used to analyze the cytokines generated following treatment of human normal monocytes with exosomes. RESULTS: The GSC-secreted exosomes were preferentially absorbed by CD14+ monocytes and Gr-1+ derived myeloid cells isolated from healthy volunteers and/or glioblastoma patients. When activated, CD4+ and CD8+ T cells could also uptake GSC-secreted exosomes. Confocal microscopy revealed that only monocytes could internalize GSC-secreted exosomes but not fibroblast-secreted exosomes. The exposure to GSC-secreted exosomes induces a phenotypic change in monocytes and prevents them from undergoing apoptosis. GSC-secreted exosomes, but not the fibroblast-secreted exosomes, increased expression of CD163, CD206, and decreased expression of MHC class II. Monocytes treated with GSC-secreted exosomes release IL-6, IL-1RA, CCL3, and CCL4 when compared to cells exposed to fibroblast exosomes. GSC-secreted exosomes contained distinct protein composition in contrast to fibroblast-secreted exosomes that may affect the anti-tumor function of monocyte-derived macrophages. CONCLUSIONS: Monocytes demonstrated a preferential uptake of GSC-secreted exosomes which then induced a glioma-supportive M2 phenotype. GSC-secreted exosomes can be a contributing factor in the M2 skewing within glioma microenvironment.
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