Evidence map›Paper›PMID 22315226›Full record

ArticleThe Journal of biological chemistry2012

The cell surface glycoprotein CUB domain-containing protein 1 (CDCP1) contributes to epidermal growth factor receptor-mediated cell migration.

Ying Dong, Yaowu He, Leonore de Boer, M Sharon Stack, John W Lumley, Judith A Clements, John D Hooper

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 62 citations in OpenAlex.

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  20. CD318 is a ligand for CD6.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

7 authors at 3 institutions in 2 countries.

Ying DongCancer Research Program, Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, Queensland 4059, Australia.
Yaowu HeMater Medical Research Institute, South Brisbane, Queensland 4101, Australia.
Leonore de BoerCancer Research Program, Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, Queensland 4059, Australia.
M Sharon StackDepartment of Pathology and Anatomical Sciences, University of Missouri, Columbia, Missouri 65212, and.
John W LumleyWesley Medical Centre, Auchenflower, Queensland 4066, Australia.
Judith A ClementsCancer Research Program, Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, Queensland 4059, Australia.
John D HooperMater Medical Research Institute, South Brisbane, Queensland 4101, Australia,. Electronic address: jhooper@mmri.mater.org.au.
Mater Research · AUUniversity of Missouri · USWesley Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor (EGF) activation of the EGF receptor (EGFR) is an important mediator of cell migration, and aberrant signaling via this system promotes a number of malignancies including ovarian cancer. We have identified the cell surface glycoprotein CDCP1 as a key regulator of EGF/EGFR-induced cell migration. We show that signaling via EGF/EGFR induces migration of ovarian cancer Caov3 and OVCA420 cells with concomitant up-regulation of CDCP1 mRNA and protein. Consistent with a role in cell migration CDCP1 relocates from cell-cell junctions to punctate structures on filopodia after activation of EGFR. Significantly, disruption of CDCP1 either by silencing or the use of a function blocking antibody efficiently reduces EGF/EGFR-induced cell migration of Caov3 and OVCA420 cells. We also show that up-regulation of CDCP1 is inhibited by pharmacological agents blocking ERK but not Src signaling, indicating that the RAS/RAF/MEK/ERK pathway is required downstream of EGF/EGFR to induce increased expression of CDCP1. Our immunohistochemical analysis of benign, primary, and metastatic serous epithelial ovarian tumors demonstrates that CDCP1 is expressed during progression of this cancer. These data highlight a novel role for CDCP1 in EGF/EGFR-induced cell migration and indicate that targeting of CDCP1 may be a rational approach to inhibit progression of cancers driven by EGFR signaling including those resistant to anti-EGFR drugs because of activating mutations in the RAS/RAF/MEK/ERK pathway.

Indexed as

Cell MovementGene Expression Regulation, NeoplasticAntigens, CDAntigens, NeoplasmAntineoplastic AgentsCell Adhesion MoleculesCell Line, TumorDrug Resistance, NeoplasmEpidermal Growth FactorErbB ReceptorsFemaleHumansIntercellular JunctionsMAP Kinase Signaling SystemMutationNeoplasm ProteinsAntigens, CDAntigens, NeoplasmAntineoplastic AgentsCDCP1 protein, humanCell Adhesion MoleculesEGFR protein, humanEpidermal Growth FactorErbB ReceptorsNeoplasm ProteinsRNA, MessengerRNA, Neoplasm

Identifiers

PMID22315226
PMCPMC3322992
OpenAlexW2054965736

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.