Evidence map›Paper›PMID 19671673›Full record

ArticleMolecular cancer research : MCR2009

Functional role of cell surface CUB domain-containing protein 1 in tumor cell dissemination.

Elena I Deryugina, Erin M Conn, Andreas Wortmann, Juneth J Partridge, Tatyana A Kupriyanova, Veronica C Ardi, John D Hooper, James P Quigley

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 62 citations in OpenAlex.

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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

8 authors at 2 institutions in 2 countries.

Elena I DeryuginaDepartment of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Erin M Conn
Andreas Wortmann
Juneth J Partridge
Tatyana A Kupriyanova
Veronica C Ardi
John D Hooper
James P Quigley
Scripps Research Institute · USQueensland University of Technology · AU

Funding

Transmembrane Proteins Involved in Human Tumor ExpansionR01CA105412 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI QUIGLEY, JAMES P · 2004 to 2020
$5.8M
BLOOD SYSTEMS IN COAGULATION AND VESSEL DISEASET32HL007195 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI RUF, WOLFRAM · 1985 to 2011
$5.1M
A Cellular and Molecular Analysis of the Intravasation Step in Tumor MetastasisR01CA129484 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI QUIGLEY, JAMES P · 2008 to 2012
$2.3M
MOLECULAR PATHOLOGY OF CANCER TRAINING GRANTT32CA077109 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KAMPS, MARK P · 1998 to 2009
$1.2M
NCI NIH HHS CA105412NCI NIH HHS CA129484NCI NIH HHS R01 CA105412NCI NIH HHS R01 CA129484NCI NIH HHS T32 CA077109NCI NIH HHS T32CA77109-08NHLBI NIH HHS T32 HL007195NHLBI NIH HHS T32HL07195
6 · The paper itself

Abstract

The function of CUB domain-containing protein 1 (CDCP1), a recently described transmembrane protein expressed on the surface of hematopoietic stem cells and normal and malignant cells of different tissue origin, is not well defined. The contribution of CDCP1 to tumor metastasis was analyzed by using HeLa carcinoma cells overexpressing CDCP1 (HeLa-CDCP1) and a high-disseminating variant of prostate carcinoma PC-3 naturally expressing high levels of CDCP1 (PC3-hi/diss). CDCP1 expression rendered HeLa cells more aggressive in experimental metastasis in immunodeficient mice. Metastatic colonization by HeLa-CDCP1 was effectively inhibited with subtractive immunization-generated, CDCP1-specific monoclonal antibody (mAb) 41-2, suggesting that CDCP1 facilitates relatively late stages of the metastatic cascade. In the chick embryo model, time- and dose-dependent inhibition of HeLa-CDCP1 colonization by mAb 41-2 was analyzed quantitatively to determine when and where CDCP1 functions during metastasis. Quantitative PCR and immunohistochemical analyses indicated that CDCP1 facilitated tumor cell survival soon after vascular arrest. Live cell imaging showed that the function-blocking mechanism of mAb 41-2 involved enhancement of tumor cell apoptosis, confirmed by attenuation of mAb 41-2-mediated effects with the caspase inhibitor z-VAD-fmk. Under proapoptotic conditions in vitro, CDCP1 expression conferred HeLa-CDCP1 cells with resistance to doxorubicin-induced apoptosis, whereas ligation of CDCP1 with mAb 41-2 caused additional enhancement of the apoptotic response. The functional role of naturally expressed CDCP1 was shown by mAb 41-2-mediated inhibition of both experimental and spontaneous metastasis of PC3-hi/diss. These findings confirm that CDCP1 functions as an antiapoptotic molecule and indicate that during metastasis CDCP1 facilitates tumor cell survival likely during or soon after extravasation.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, CDAntigens, NeoplasmApoptosisCell Adhesion MoleculesCell MembraneCell ShapeChick EmbryoDisease Models, AnimalDoxorubicinHeLa CellsHumansKineticsMaleMiceAntibodies, MonoclonalAntigens, CDAntigens, NeoplasmCDCP1 protein, humanCell Adhesion MoleculesDoxorubicinNeoplasm ProteinsPhosphotyrosine

Identifiers

PMID19671673
PMCPMC3068911
OpenAlexW2102944450

What OpenQuestion holds

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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.