Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2. Dwyer, J., Hebda, J. K., Le Guelte, A., Galan-Moya, E. M., Smith, S. S., Azzi, S., Bidere, N., & Gavard, J. PLoS One, 7(9):e45562, 2012. ![Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2 [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper abstract bibtex Glioblastoma constitutes the most aggressive and deadly of brain tumors. As yet, both conventional and molecular-based therapies have met with limited success in treatment of this cancer. Among other explanations, the heterogeneity of glioblastoma and the associated microenvironment contribute to its development, as well as resistance and recurrence in response to treatments. Increased vascularity suggests that tumor angiogenesis plays an important role in glioblastoma progression. However, the molecular crosstalk between endothelial and glioblastoma cells requires further investigation. To examine the effects of glioblastoma-derived signals on endothelial homeostasis, glioblastoma cell secretions were collected and used to treat brain endothelial cells. Here, we present evidence that the glioblastoma secretome provides pro-angiogenic signals sufficient to disrupt VE-cadherin-mediated cell-cell junctions and promote endothelial permeability in brain microvascular endothelial cells. An unbiased angiogenesis-specific antibody array screen identified the chemokine, interleukin-8, which was further demonstrated to function as a key factor involved in glioblastoma-induced permeability, mediated through its receptor CXCR2 on brain endothelia. This underappreciated interface between glioblastoma cells and associated endothelium may inspire the development of novel therapeutic strategies to induce tumor regression by preventing vascular permeability and inhibiting angiogenesis.
@article{dwyer_glioblastoma_2012,
title = {Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via {CXCR2}},
volume = {7},
issn = {1932-6203 (ELECTRONIC) 1932-6203 (LINKING)},
shorttitle = {Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via {CXCR2}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/23029099},
abstract = {Glioblastoma constitutes the most aggressive and deadly of brain tumors. As yet, both conventional and molecular-based therapies have met with limited success in treatment of this cancer. Among other explanations, the heterogeneity of glioblastoma and the associated microenvironment contribute to its development, as well as resistance and recurrence in response to treatments. Increased vascularity suggests that tumor angiogenesis plays an important role in glioblastoma progression. However, the molecular crosstalk between endothelial and glioblastoma cells requires further investigation. To examine the effects of glioblastoma-derived signals on endothelial homeostasis, glioblastoma cell secretions were collected and used to treat brain endothelial cells. Here, we present evidence that the glioblastoma secretome provides pro-angiogenic signals sufficient to disrupt VE-cadherin-mediated cell-cell junctions and promote endothelial permeability in brain microvascular endothelial cells. An unbiased angiogenesis-specific antibody array screen identified the chemokine, interleukin-8, which was further demonstrated to function as a key factor involved in glioblastoma-induced permeability, mediated through its receptor CXCR2 on brain endothelia. This underappreciated interface between glioblastoma cells and associated endothelium may inspire the development of novel therapeutic strategies to induce tumor regression by preventing vascular permeability and inhibiting angiogenesis.},
number = {9},
journal = {PLoS One},
author = {Dwyer, J. and Hebda, J. K. and Le Guelte, A. and Galan-Moya, E. M. and Smith, S. S. and Azzi, S. and Bidere, N. and Gavard, J.},
year = {2012},
keywords = {Brain Neoplasms/genetics/*metabolism *Capillary Permeability/drug effects Cell Line, Conditioned/pharmacology Endothelial Cells/drug effects/*metabolism Gene Expression Regulation, Interleukin-8B/genetics/*metabolism, Neoplastic Glioblastoma/genetics/*metabolism Humans Interleukin-8/pharmacology/*secretion Receptors, Tumor Culture Media},
pages = {e45562},
}
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Among other explanations, the heterogeneity of glioblastoma and the associated microenvironment contribute to its development, as well as resistance and recurrence in response to treatments. Increased vascularity suggests that tumor angiogenesis plays an important role in glioblastoma progression. However, the molecular crosstalk between endothelial and glioblastoma cells requires further investigation. To examine the effects of glioblastoma-derived signals on endothelial homeostasis, glioblastoma cell secretions were collected and used to treat brain endothelial cells. Here, we present evidence that the glioblastoma secretome provides pro-angiogenic signals sufficient to disrupt VE-cadherin-mediated cell-cell junctions and promote endothelial permeability in brain microvascular endothelial cells. An unbiased angiogenesis-specific antibody array screen identified the chemokine, interleukin-8, which was further demonstrated to function as a key factor involved in glioblastoma-induced permeability, mediated through its receptor CXCR2 on brain endothelia. 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