Evidence map›Paper›PMID 29203859›Full record

ArticleNature communications2017

Interleukin-13 receptor alpha 2 cooperates with EGFRvIII signaling to promote glioblastoma multiforme.

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 and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 91 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 9 institutions in 4 countries.

Jennifer P NewmanLaboratory of Cancer Gene Therapy, Cellular and Molecular Research Division, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore, 169610, Singapore.
Grace Y WangLaboratory of Cancer Gene Therapy, Cellular and Molecular Research Division, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore, 169610, Singapore.
Kazuhiko ArimaDepartment of Biomolecular Sciences, Saga Medical School, Saga, 840-8502, Japan.
Shou P GuanLaboratory of Cancer Gene Therapy, Cellular and Molecular Research Division, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore, 169610, Singapore.
Michael R WatersSchool of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Webster K CaveneeLudwig Institute for Cancer Research, San Diego, CA, 92093, USA.
Edward PanDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Edita AliwargaLaboratory of Cancer Gene Therapy, Cellular and Molecular Research Division, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore, 169610, Singapore.
Siao T ChongLaboratory of Cancer Gene Therapy, Cellular and Molecular Research Division, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore, 169610, Singapore.
Catherine Y L KokLaboratory of Cancer Gene Therapy, Cellular and Molecular Research Division, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore, 169610, Singapore.
Berwini B EndayaSchool of Medical Science, Griffith Health Institute, Griffith University, Southport, 4222, Queensland, Australia.
Amyn A HabibDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center and the North Texas VA Medical Center, Dallas, 75390, USA.ORCID http://orcid.org/0000-0003-4164-9028
Tomohisa HoribeDepartment of Pharmacoepidemiology, Kyoto University School of Public Health, Kyoto, 606-8501, Japan.
Wai H NgNational Neuroscience Institute, 11 Jalan Tan Tock Seng, Singapore, 308433, Singapore.
Ivy A W HoLaboratory of Cancer Gene Therapy, Cellular and Molecular Research Division, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore, 169610, Singapore.
Kam M HuiBek Chai Heah Laboratory of Cancer Genomics, Cellular and Molecular Research Division, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore, 169610, Singapore.
Tomasz KordulaSchool of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Paula Y P LamLaboratory of Cancer Gene Therapy, Cellular and Molecular Research Division, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore, 169610, Singapore. phslypp@nus.edu.sg.
National Cancer Centre Singapore · SGNational Neuroscience Institute · SGNational University of Singapore · SGVirginia Commonwealth University · USDallas VA Medical Center · USGriffith University · AUKyoto University · JPLudwig Cancer Research · USThe University of Texas Southwestern Medical Center · US

Funding

Novel Functions of S1P in NeuroinflammationR01AI093718 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI KORDULA, TOMASZ K · 2012 to 2016
$1.8M
Interactions between inflammatory and oncogenic signaling pathways in GBMI01BX002559 · VA · VA NORTH TEXAS HEALTH CARE SYSTEM · PI HABIB, AMYN · 2014 to 2021
–
BLRD VA I01 BX002559NIAID NIH HHS R01 AI093718
6 · The paper itself

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.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorCell ProliferationErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGene Knockdown TechniquesGlioblastomaHumansInterleukin-13 Receptor alpha2 SubunitIn Vitro TechniquesMAP Kinase Kinase KinasesMiceMutationNeoplasm InvasivenessNeoplasm Transplantationepidermal growth factor receptor VIIIErbB ReceptorsExtracellular Signal-Regulated MAP KinasesInterleukin-13 Receptor alpha2 SubunitMAP Kinase Kinase Kinasesraf Kinasesras ProteinsRNA, Messenger

Identifiers

PMID29203859
PMCPMC5715073
OpenAlexW2769408674

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.