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Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE138115 | GEO | 2019/12/20

REPOSITORIES: GEO

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Glioma-Derived miRNA-Containing Extracellular Vesicles Induce Angiogenesis by Reprogramming Brain Endothelial Cells.

Project description:Glioblastoma (GBM) is characterized by aberrant vascularization and a complex tumor microenvironment. The failure of anti-angiogenic therapies suggests pathways of GBM neovascularization, possibly attributable to glioblastoma stem cells (GSCs) and their interplay with the tumor microenvironment. It has been established that GSC-derived extracellular vesicles (GSC-EVs) and their cargoes are proangiogenic in vitro. To further elucidate EV-mediated mechanisms of neovascularization in vitro, we perform RNA-seq and DNA methylation profiling of human brain endothelial cells exposed to GSC-EVs. To correlate these results to tumors in vivo, we perform histoepigenetic analysis of GBM molecular profiles in the TCGA collection. Remarkably, GSC-EVs and normal vascular growth factors stimulate highly distinct gene regulatory responses that converge on angiogenesis. The response to GSC-EVs shows a footprint of post-transcriptional gene silencing by EV-derived miRNAs. Our results provide insights into targetable angiogenesis pathways in GBM and miRNA candidates for liquid biopsy biomarkers.

| S-EPMC7148092 | biostudies-literature

Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells (miRNA-seq)

Project description:Glioblastoma multiforme (GBM) is characterized by the close relationship of glioma stem cells (GSC) with aberrant vascularization. It has been established that GSC-derived extracellular vesicles (GSC-EVs) and their cargoes are proangiogenic in vitro. To elucidate gene regulatory mechanisms of neovascularization both in vitro and in vivo, we performed RNA-seq and DNA methylation profiling of the response of human brain endothelial cells to GSC-EVs as well as histoepigenetic analysis of GBM molecular profiles in the TCGA collection. The gene regulatory responses showed a footprint of post-transcriptional gene silencing by EV-derived miRNAs. Remarkably, EVs and normal vascular growth factors stimulated highly distinct gene regulatory responses, both converging on angiogenesis, providing exciting new insight into targetable angiogenic signaling in GBM.

2019-12-20 | GSE138114 | GEO

Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells (longRNA-seq)

2019-12-20 | GSE138113 | GEO

Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells (DNA methylation)

2019-12-20 | GSE137830 | GEO

Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells

Project description:Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells

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Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells (miRNA-seq)

Project description:Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells (miRNA-seq)

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Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells (longRNA-seq)

Project description:Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells (longRNA-seq)

| PRJNA574644 | ENA

Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells (DNA methylation)

Project description:Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells (DNA methylation)

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Extracellular vesicles from Kaposi Sarcoma-associated herpesvirus lymphoma induce long-term endothelial cell reprogramming.

Project description:Extracellular signaling is a mechanism that higher eukaryotes have evolved to facilitate organismal homeostasis. Recent years have seen an emerging interest in the role of secreted microvesicles, termed extracellular vesicles (EV) or exosomes in this signaling network. EV contents can be modified by the cell in response to stimuli, allowing them to relay information to neighboring cells, influencing their physiology. Here we show that the tumor virus Kaposi's Sarcoma-associated herpesvirus (KSHV) hijacks this signaling pathway to induce cell proliferation, migration, and transcriptome reprogramming in cells not infected with the virus. KSHV-EV activates the canonical MEK/ERK pathway, while not alerting innate immune regulators, allowing the virus to exert these changes without cellular pathogen recognition. Collectively, we propose that KSHV establishes a niche favorable for viral spread and cell transformation through cell-derived vesicles, all while avoiding detection.

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Extracellular Vesicles Containing MicroRNA-92a-3p Facilitate Partial Endothelial-Mesenchymal Transition and Angiogenesis in Endothelial Cells.

Project description:Extracellular vesicles (EVs) are nanometer-sized membranous vesicles used for primitive cell-to-cell communication. We previously reported that colon cancer-derived EVs contain abundant miR-92a-3p and have a pro-angiogenic function. We previously identified Dickkopf-3 (Dkk-3) as a direct target of miR-92a-3p; however, the pro-angiogenic function of miR-92a-3p cannot only be attributed to downregulation of Dkk-3. Therefore, the complete molecular mechanism by which miR-92a-3p exerts pro-angiogenic effects is still unclear. Here, we comprehensively analyzed the gene sets affected by ectopic expression of miR-92a-3p in endothelial cells to elucidate processes underlying EV-induced angiogenesis. We found that the ectopic expression of miR-92a-3p upregulated cell cycle- and mitosis-related gene expression and downregulated adhesion-related gene expression in endothelial cells. We also identified a novel target gene of miR-92a-3p, claudin-11. Claudin-11 belongs to the claudin gene family, which encodes essential components expressed at tight junctions (TJs). Disruption of TJs with a concomitant loss of claudin expression is a significant event in the process of epithelial-to-mesenchymal transition. Our findings have unveiled a new EV-mediated mechanism for tumor angiogenesis through the induction of partial endothelial-to-mesenchymal transition in endothelial cells.

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