Evidence map›Paper›PMID 24980826›Full record

ArticleOncotarget2014

Urokinase receptor promotes ovarian cancer cell dissemination through its 84-95 sequence.

Katia Bifulco, Giuseppina Votta, Vincenzo Ingangi, Gioconda Di Carluccio, Domenica Rea, Simona Losito, Nunzia Montuori, Pia Ragno, Maria Patrizia Stoppelli, Claudio Arra and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 19 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

11 authors at 4 institutions in 1 country.

Katia BifulcoDepartment of Experimental Oncology Unit, IRCCS Istituto Nazionale Tumori "Fondazione G. Pascale", Naples, Italy.
Giuseppina VottaDepartment of Experimental Pathology Unit, IRCCS Istituto Nazionale Tumori "Fondazione G. Pascale", Naples, Italy.
Vincenzo IngangiDepartment of Experimental Oncology Unit, IRCCS Istituto Nazionale Tumori "Fondazione G. Pascale", Naples, Italy.
Gioconda Di CarluccioDepartment of Experimental Oncology Unit, IRCCS Istituto Nazionale Tumori "Fondazione G. Pascale", Naples, Italy.
Domenica ReaDepartment of Experimental Oncology Unit, IRCCS Istituto Nazionale Tumori "Fondazione G. Pascale", Naples, Italy.
Simona LositoInstitute of Genetics and Biophysics "Adriano Buzzati-Traverso", National Research Council, Naples, Italy.
Nunzia MontuoriDepartment of Translational Medical Sciences,''Federico II'' University, Naples, Italy.
Pia RagnoDepartment of Chemistry and Biology, University of Salerno, Fisciano (Salerno), Italy.
Maria Patrizia StoppelliDepartment of Experimental Pathology Unit, IRCCS Istituto Nazionale Tumori "Fondazione G. Pascale", Naples, Italy.
Claudio ArraDepartment of Experimental Oncology Unit, IRCCS Istituto Nazionale Tumori "Fondazione G. Pascale", Naples, Italy. These authors contributed equally.
Maria Vincenza CarrieroDepartment of Experimental Oncology Unit, IRCCS Istituto Nazionale Tumori "Fondazione G. Pascale", Naples, Italy. These authors contributed equally.
Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITFederico II University Hospital · ITNational Research Council · ITUniversity of Salerno · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The clinical relevance of the urokinase receptor (uPAR) as a prognostic marker in ovarian cancer is well documented. We had shown that the uPAR sequence corresponding to 84-95 residues, linking D1 and D2 domains (uPAR84-95), drives cell migration and angiogenesis in a protease-independent manner. This study was aimed at defining the contribution of uPAR84-95 sequence to invasion of ovarian cancer cells. Now, we provide evidence that the ability of uPAR-expressing ovarian cancer cells to cross extra-cellular matrix and mesothelial monolayers is prevented by specific inhibitors of the uPAR84-95 sequence. To specifically investigate uPAR84-95 function, uPAR-negative CHO-K1 cells were stably transfected with cDNAs coding for uPAR D2 and D3 regions exposing (uPARD2D3) or lacking (uPAR∆D2D3) the 84-95 sequence. CHO-K1/D2D3 cells were able to cross matrigel, mesothelial and endothelial monolayers more efficiently than CHO-K1/∆D2D3 cells, which behave as CHO-K1 control cells. When orthotopically implanted in nude mice, tumor nodules generated by CHO-K1/D2D3 cells spreading to peritoneal cavity were more numerous as compared to CHO-K1/∆D2D3 cells. Ovarian tumor size and intra-tumoral microvessel density were significantly reduced in the absence of uPAR84-95. Our results indicate that cell associated uPAR promotes growth and abdominal dissemination of ovarian cancer cells mainly through its uPAR84-95 sequence.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationFemaleHumansMiceMice, NudeOvarian NeoplasmsPrognosisReceptors, Urokinase Plasminogen ActivatorTransfectionReceptors, Urokinase Plasminogen Activator

Identifiers

PMID24980826
PMCPMC4147313
OpenAlexW2146691900

What OpenQuestion holds

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Registered trials

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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.