Evidence map›Paper›PMID 25874673›Full record

ArticleNature2015

The Drosophila TNF receptor Grindelwald couples loss of cell polarity and neoplastic growth.

Ditte S Andersen, Julien Colombani, Valentina Palmerini, Krittalak Chakrabandhu, Emilie Boone, Michael Röthlisberger, Janine Toggweiler, Konrad Basler, Marina Mapelli, Anne-Odile Hueber and 1 more

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In one paragraph

Article in Nature, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

112 citing papers in PubMed, 177 citations in OpenAlex.

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  11. Glial-derived TNF/Eiger signaling promotes somatosensory neurite sculpting.Cellular and molecular life sciences : CMLS · 2025
    Article
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52 more citing papers are in PubMed but not listed here.

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 3 countries.

Ditte S Andersen1] University of Nice-Sophia Antipolis, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [2] CNRS, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [3] INSERM, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [4] Genetics and Physiology of Growth laboratory, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France.
Julien Colombani1] University of Nice-Sophia Antipolis, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [2] CNRS, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [3] INSERM, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [4] Genetics and Physiology of Growth laboratory, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France.
Valentina PalmeriniDepartment of Experimental Oncology, European Institute of Oncology, Via Adamello 16, 20139 Milan, Italy.
Krittalak Chakrabandhu1] University of Nice-Sophia Antipolis, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [2] CNRS, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [3] INSERM, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [4] Death receptors Signalling and Cancer Therapy laboratory, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France.
Emilie Boone1] University of Nice-Sophia Antipolis, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [2] CNRS, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [3] INSERM, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [4] Genetics and Physiology of Growth laboratory, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France.
Michael RöthlisbergerInstitute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Janine ToggweilerInstitute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Konrad BaslerInstitute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Marina MapelliDepartment of Experimental Oncology, European Institute of Oncology, Via Adamello 16, 20139 Milan, Italy.
Anne-Odile Hueber1] University of Nice-Sophia Antipolis, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [2] CNRS, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [3] INSERM, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [4] Death receptors Signalling and Cancer Therapy laboratory, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France.
Pierre Léopold1] University of Nice-Sophia Antipolis, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [2] CNRS, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [3] INSERM, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France [4] Genetics and Physiology of Growth laboratory, Institute of Biology Valrose, Parc Valrose, 06108 Nice, France.
Centre National de la Recherche Scientifique · FRInstitut de Biologie Valrose · FRUniversity of Zurich · CHEuropean Institute of Oncology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption of epithelial polarity is a key event in the acquisition of neoplastic growth. JNK signalling is known to play an important part in driving the malignant progression of many epithelial tumours, although the link between loss of polarity and JNK signalling remains elusive. In a Drosophila genome-wide genetic screen designed to identify molecules implicated in neoplastic growth, we identified grindelwald (grnd), a gene encoding a transmembrane protein with homology to members of the tumour necrosis factor receptor (TNFR) superfamily. Here we show that Grnd mediates the pro-apoptotic functions of Eiger (Egr), the unique Drosophila TNF, and that overexpression of an active form of Grnd lacking the extracellular domain is sufficient to activate JNK signalling in vivo. Grnd also promotes the invasiveness of Ras(V12)/scrib(-/-) tumours through Egr-dependent Matrix metalloprotease-1 (Mmp1) expression. Grnd localizes to the subapical membrane domain with the cell polarity determinant Crumbs (Crb) and couples Crb-induced loss of polarity with JNK activation and neoplastic growth through physical interaction with Veli (also known as Lin-7). Therefore, Grnd represents the first example of a TNFR that integrates signals from both Egr and apical polarity determinants to induce JNK-dependent cell death or tumour growth.

Indexed as

Cell PolarityAmino Acid SequenceAnimalsApoptosisCell Adhesion MoleculesCell DivisionCell Transformation, NeoplasticDisease Models, AnimalDrosophila melanogasterDrosophila ProteinsFemaleHumansJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Signaling SystemMatrix Metalloproteinase 1Cell Adhesion Moleculescrb protein, DrosophilaDrosophila Proteinsegr protein, Drosophilagrnd protein, DrosophilaJNK Mitogen-Activated Protein KinasesMatrix Metalloproteinase 1Membrane Proteinsras ProteinsReceptors, Tumor Necrosis FactorScrib protein, DrosophilaVeli protein, Drosophila

Identifiers

PMID25874673
OpenAlexW1982468647

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.