Interleukin-13 receptor alpha 2 cooperates with EGFRvIII signaling to promote glioblastoma multiforme View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Jennifer P. Newman, Grace Y. Wang, Kazuhiko Arima, Shou P. Guan, Michael R. Waters, Webster K. Cavenee, Edward Pan, Edita Aliwarga, Siao T. Chong, Catherine Y. L. Kok, Berwini B. Endaya, Amyn A. Habib, Tomohisa Horibe, Wai H. Ng, Ivy A. W. Ho, Kam M. Hui, Tomasz Kordula, Paula Y. P. Lam

ABSTRACT

The interleukin-13 receptor alpha2 (IL-13Rα2) is a cancer-associated receptor overexpressed in human glioblastoma multiforme (GBM). This receptor is undetectable in normal brain which makes it a highly suitable target for diagnostic and therapeutic purposes. However, the pathological role of this receptor in GBM remains to be established. Here we report that IL-13Rα2 alone induces invasiveness of human GBM cells without affecting their proliferation. In contrast, in the presence of the mutant EGFR (EGFRvIII), IL-13Rα2 promotes GBM cell proliferation in vitro and in vivo. Mechanistically, the cytoplasmic domain of IL-13Rα2 specifically binds to EGFRvIII, and this binding upregulates the tyrosine kinase activity of EGFRvIII and activates the RAS/RAF/MEK/ERK and STAT3 pathways. Our findings support the "To Go or To Grow" hypothesis whereby IL-13Rα2 serves as a molecular switch from invasion to proliferation, and suggest that targeting both receptors with STAT3 signaling inhibitor might be a therapeutic approach for the treatment of GBM. More... »

PAGES

1913

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-017-01392-9

    DOI

    http://dx.doi.org/10.1038/s41467-017-01392-9

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1093066649

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/29203859


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