Evidence map›Paper›PMID 24644285›Full record

ArticleThe Journal of biological chemistry2014

Epithelial membrane protein-2 (EMP2) activates Src protein and is a novel therapeutic target for glioblastoma.

Yu Qin, Maoyong Fu, Masamichi Takahashi, Akio Iwanami, Daisuke Kuga, Rajiv G Rao, Deepthi Sudhakar, Tiffany Huang, Meagan Kiyohara, Kathleen Torres and 8 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 23% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. A recurrent de novo damaging variant inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. EMP3: A promising biomarker for tumor prognosis and targeted cancer therapy.Cancer biomarkers : section A of Disease markers · 2024
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Genetic Deletion ofFrontiers in medicine · 2019
    Article
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 3 institutions in 1 country.

Yu QinFrom the Departments of Ophthalmology and.
Maoyong FuPathology and Laboratory Medicine.
Masamichi TakahashiDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 90095 and.
Akio IwanamiPathology and Laboratory Medicine.
Daisuke KugaPathology and Laboratory Medicine.
Rajiv G RaoPathology and Laboratory Medicine.
Deepthi SudhakarPathology and Laboratory Medicine.
Tiffany HuangPathology and Laboratory Medicine.
Meagan KiyoharaPathology and Laboratory Medicine.
Kathleen TorresPathology and Laboratory Medicine.
Christen DillardPathology and Laboratory Medicine.
Akihito InagakiDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 90095 and.
Noriyuki KasaharaDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 90095 and.
Lee GoodglickPathology and Laboratory Medicine, Jonsson Comprehensive Cancer Center, and.
Jonathan BraunPathology and Laboratory Medicine, Jonsson Comprehensive Cancer Center, and.
Paul S Mischelthe Ludwig Institute for Cancer Research, Department of Pathology, University of California at San Diego, La Jolla, California 92093.
Lynn K GordonFrom the Departments of Ophthalmology and.
Madhuri WadehraPathology and Laboratory Medicine, Jonsson Comprehensive Cancer Center, and mwadehra@mednet.ucla.edu.
University of California, Los Angeles · USUCLA Jonsson Comprehensive Cancer CenterUniversity of California, San Diego · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ANTON, PETER A · 1991 to 2018
$39.9M
Supporting African American Churches to Promote Cancer ScreeningU54CA143931 · NCI · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI VADGAMA, JAYDUTT V. · 2009 to 2022
$19.7M
Training and Mentoring ProgramsU54CA143930 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PIETRAS, RICHARD JOSEPH · 2009 to 2020
$7.5M
The Early Detection Research Network Biomarker Resource Laboratory at UCLAU24CA086366 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHIA, DAVID S. · 2000 to 2014
$7.3M
Using EMP2 for Image Guided Drug Delivery for Breast CancerR01CA163971 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OLAFSEN, TOVE, WADEHRA, MADHURI · 2012 to 2016
$1.6M
NCATS NIH HHS UL1 TR000124NCI NIH HHS CA 143931CDUNCI NIH HHS CA-86366NCI NIH HHS P30 CA016042NCI NIH HHS R01 CA163971NCI NIH HHS R01CA163971NCI NIH HHS U24 CA086366NCI NIH HHS U54 CA143930NCI NIH HHS U54 CA143931NIAID NIH HHS 5P30 AI028697NIAID NIH HHS P30 AI028697
6 · The paper itself

Abstract

Despite recent advances in molecular classification, surgery, radiotherapy, and targeted therapies, the clinical outcome of patients with malignant brain tumors remains extremely poor. In this study, we have identified the tetraspan protein epithelial membrane protein-2 (EMP2) as a potential target for glioblastoma (GBM) killing. EMP2 had low or undetectable expression in normal brain but was highly expressed in GBM as 95% of patients showed some expression of the protein. In GBM cells, EMP2 enhanced tumor growth in vivo in part by up-regulating αvβ3 integrin surface expression, activating focal adhesion kinase and Src kinases, and promoting cell migration and invasion. Consistent with these findings, EMP2 expression significantly correlated with activated Src kinase in patient samples and promoted tumor cell invasion using intracranial mouse models. As a proof of principle to determine whether EMP2 could serve as a target for therapy, cells were treated using specific anti-EMP2 antibody reagents. These reagents were effective in killing GBM cells in vitro and in reducing tumor load in subcutaneous mouse models. These results support the role of EMP2 in the pathogenesis of GBM and suggest that anti-EMP2 treatment may be a novel therapeutic treatment.

Indexed as

Molecular Targeted TherapyAnimalsCell Line, TumorCell ProliferationEnzyme ActivationFemaleFocal Adhesion Kinase 1Gene Expression Regulation, NeoplasticGlioblastomaHumansMembrane GlycoproteinsMicePhenotypesrc-Family KinasesEMP2 protein, humanFocal Adhesion Kinase 1Membrane Glycoproteinssrc-Family KinasesCell InvasionEMP2GlioblastomaImmunotherapyTetraspaninsTumor Marker

Identifiers

PMID24644285
PMCPMC4022868
OpenAlexW1991234390

What OpenQuestion holds

Textmetadata
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.