Glycosylated extracellular vesicles released by glioblastoma cells are decorated by CCL18 allowing for cellular uptake via chemokine receptor CCR8
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Author
Berenguer, Jordi
Lagerweij, Tonny
Zhao, Xi Wen
Dusoswa, Sophie
van der Stoop, Petra
Westerman, Bart
de Gooijer, Mark C.
Zoetemelk, Marloes
Zomer, Anoek
Crommentuijn, Matheus H. W.
Wedekind, Laurine E.
López-López, Àlan
Giovanazzi, Alberta
Bruch-Oms, Marina
van der Meulen-Muileman, Ida H.
Reijmers, Rogier M.
van Kuppevelt, Toin H.
García-Vallejo, Juan-Jesús
van Kooyk, Yvette
Wesseling, Pieter
Koppers-Lalic, Danijela
Vandertop, W. Peter
Noske, David P.
van Beusechem, Victor W.
van Rheenen, Jacco
Pegtel, D. Michiel
van Tellingen, Olaf
Wurdinger, Thomas
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1080/20013078.2018.1446660Metadata
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Berenguer, J., T. Lagerweij, X. W. Zhao, S. Dusoswa, P. van der Stoop, B. Westerman, M. C. de Gooijer, et al. 2018. “Glycosylated extracellular vesicles released by glioblastoma cells are decorated by CCL18 allowing for cellular uptake via chemokine receptor CCR8.” Journal of Extracellular Vesicles 7 (1): 1446660. doi:10.1080/20013078.2018.1446660. http://dx.doi.org/10.1080/20013078.2018.1446660.Abstract
ABSTRACT Cancer cells release extracellular vesicles (EVs) that contain functional biomolecules such as RNA and proteins. EVs are transferred to recipient cancer cells and can promote tumour progression and therapy resistance. Through RNAi screening, we identified a novel EV uptake mechanism involving a triple interaction between the chemokine receptor CCR8 on the cells, glycans exposed on EVs and the soluble ligand CCL18. This ligand acts as bridging molecule, connecting EVs to cancer cells. We show that glioblastoma EVs promote cell proliferation and resistance to the alkylating agent temozolomide (TMZ). Using in vitro and in vivo stem-like glioblastoma models, we demonstrate that EV-induced phenotypes are neutralised by a small molecule CCR8 inhibitor, R243. Interference with chemokine receptors may offer therapeutic opportunities against EV-mediated cross-talk in glioblastoma.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5912193/pdf/Terms of Use
This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAACitable link to this page
http://nrs.harvard.edu/urn-3:HUL.InstRepos:37067891
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