Evidence map›Paper›PMID 30843637›Full record

ArticleCancer science2019

Nectin-2 in ovarian cancer: How is it expressed and what might be its functional role?

Inga Bekes, Sanja Löb, Iris Holzheu, Wolfgang Janni, Lisa Baumann, Achim Wöckel, Christine Wulff

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.6field-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

36 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Structure-guided engineering of CD112 receptor variants for optimized immunotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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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

7 authors at 2 institutions in 1 country.

Inga BekesDepartment of Obstetrics and Gynecology, University of Ulm, Ulm, Germany.
Sanja LöbDepartment of Obstetrics and Gynecology, University of Würzburg, Würzburg, Germany.
Iris HolzheuDepartment of Obstetrics and Gynecology, University of Ulm, Ulm, Germany.
Wolfgang JanniDepartment of Obstetrics and Gynecology, University of Ulm, Ulm, Germany.
Lisa BaumannDepartment of Pathology, University of Ulm, Ulm, Germany.
Achim WöckelDepartment of Obstetrics and Gynecology, University of Würzburg, Würzburg, Germany.
Christine WulffDepartment of Obstetrics and Gynecology, University of Würzburg, Würzburg, Germany.ORCID https://orcid.org/0000-0001-5827-5275
Universität Ulm · DEUniversity of Würzburg · DE

Funding

Deutsche Forschungsgemeinschaft DFG WU 319/3-2
6 · The paper itself

Abstract

Nectin-2 is an adhesion molecule that has been reported to play a role in tumor growth, metastasis and tumor angiogenesis. Herein, we investigated Nectin-2 in ovarian cancer patients and in cell culture. Tumor as well as peritoneal biopsies of 60 ovarian cancer patients and 22 controls were dual stained for Nectin-2 and CD31 using immunohistochemistry. Gene expression of Nectin-2 was quantified by real-time PCR and differences analyzed in relation to various tumor characteristics. In the serum of patients, vascular endothelial growth factor (VEGF) was quantified by ELISA. Effect of VEGF on Nectin-2 expression as well as permeability was investigated in HUVEC. In tumor biopsies, Nectin-2 protein was mainly localized in tumor cells, whereas in peritoneal biopsies, clear colocalization was found in the vasculature. T3 patients had a significantly higher percentage of positive lymph nodes and this correlated with survival. Nectin-2 was significantly upregulated in tumor biopsies in patients with lymph node metastasis and with residual tumor >1 cm after surgery. Nectin-2 expression was significantly suppressed in the peritoneal endothelium of patients associated with significantly increased VEGF serum levels. In cell culture, VEGF stimulation led to a significant downregulation of Nectin-2 which was reversed by VEGF-inhibition. In addition, Nectin-2 knockdown in endothelial cells was associated with significantly increased endothelial permeability. Nectin-2 expression in ovarian cancer may support tumor cell adhesion, leading to growth and lymph node metastasis. In addition, VEGF-induced Nectin-2 suppression in peritoneal endothelium may support an increase in vascular permeability leading to ascites production.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAged, 80 and overCapillary PermeabilityCarcinoma, Ovarian EpithelialCells, CulturedFemaleHumansHuman Umbilical Vein Endothelial CellsLymphatic MetastasisMiddle AgedNectinsOvarian NeoplasmsPeritoneumRNA InterferenceNECTIN2 protein, humanNectinsVascular Endothelial Growth FactorsmetastasisNectin-2ovarian cancersurvivalVEGF

Identifiers

PMID30843637
PMCPMC6549928
OpenAlexW2921699220

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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.