Evidence map›Paper›PMID 24558503›Full record

ArticlePloS one2014

Desmoglein 2 depletion leads to increased migration and upregulation of the chemoattractant secretoneurin in melanoma cells.

Wiebke K Peitsch, Yvette Doerflinger, Reiner Fischer-Colbrie, Volker Huck, Alexander T Bauer, Jochen Utikal, Sergij Goerdt, Stefan W Schneider

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  11. Cell Adhesion Molecules in Plasticity and Metastasis.Molecular cancer research : MCR · 2021
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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 5 institutions in 2 countries.

Wiebke K PeitschDepartment of Dermatology, University Medical Center Mannheim, Heidelberg University, Mannheim, Germany ; Helmholtz Group for Cell Biology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Yvette DoerflingerDepartment of Dermatology, University Medical Center Mannheim, Heidelberg University, Mannheim, Germany ; Helmholtz Group for Cell Biology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Reiner Fischer-ColbrieDepartment of Pharmacology, Innsbruck Medical University, Innsbruck, Austria.
Volker HuckDepartment of Dermatology, University Medical Center Mannheim, Heidelberg University, Mannheim, Germany.
Alexander T BauerDepartment of Dermatology, University Medical Center Mannheim, Heidelberg University, Mannheim, Germany.
Jochen UtikalDepartment of Dermatology, University Medical Center Mannheim, Heidelberg University, Mannheim, Germany ; Skin Cancer Unit, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Sergij GoerdtDepartment of Dermatology, University Medical Center Mannheim, Heidelberg University, Mannheim, Germany.
Stefan W SchneiderDepartment of Dermatology, University Medical Center Mannheim, Heidelberg University, Mannheim, Germany.
University Medical Centre Mannheim · DEGerman Cancer Research Center · DEHeidelberg University · DEInnsbruck Medical University · ATUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During development and progression of malignant melanoma, an important role has been attributed to alterations of cell-cell adhesions, in particular, to a "cadherin switch" from E- to N-cadherin. We have previously shown that a subtype of melanoma cells express the desmosomal cadherin desmoglein 2 as non-junction-bound cell surface protein in addition to classical cadherins. To study the role of desmoglein 2 in melanoma cells, melanoma lines containing high endogenous amounts of desmoglein 2 were depleted of the protein by RNA interference. Transwell migration and scratch wounding assays showed markedly increased migration upon desmoglein 2 suppression whereas proliferation and viability remained unaltered. In gene expression profiles, desmoglein 2 depletion was associated with overexpression of migration-related genes. Strongest overexpression was found for secretogranin II which has not been reported in melanoma cells before. The bioactive peptide derived from secretogranin II, secretoneurin, is known to exert chemoattractive functions and was demonstrated here to stimulate melanoma cell migration. In summary, we show that desmoglein 2 expression attenuates migration of melanoma cells. The mechanism of desmoglein 2 impaired cell migration is mediated by downregulation of secretogranin II. Loss of desmoglein 2 increases expression of secretogranin II, followed by an enhanced migratory activity of melanoma cells. Our data add a new pathway of regulating melanoma cell migration related to a desmoglein 2-secretogranin II axis.

Indexed as

BromodeoxyuridineCell Line, TumorCell MovementDesmoglein 2Electric ImpedanceGene Expression ProfilingGene Expression RegulationHumansImmunoblottingImmunohistochemistryMelanomaMicroscopy, FluorescenceRadioimmunoassayReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA InterferenceBromodeoxyuridineDesmoglein 2Secretogranin II

Identifiers

PMID24558503
PMCPMC3928442
OpenAlexW2084819063

What OpenQuestion holds

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LicenceCC BY
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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.