Evidence map›Paper›PMID 25391145›Full record

ArticlePloS one2014

The actin targeting compound Chondramide inhibits breast cancer metastasis via reduction of cellular contractility.

Magdalena H Menhofer, Rebekka Kubisch, Laura Schreiner, Matthias Zorn, Florian Foerster, Rolf Mueller, Joachim O Raedler, Ernst Wagner, Angelika M Vollmar, Stefan Zahler

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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

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  19. Insights From the Ecology of Information to Cancer Control.Cancer control : journal of the Moffitt Cancer Center
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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

10 authors at 2 institutions in 1 country.

Magdalena H MenhoferDepartment of Pharmacy, Pharmaceutical Biology, University of Munich, Munich, Germany.
Rebekka KubischDepartment of Pharmacy, Pharmaceutical Biotechnology, University of Munich, Munich, Germany.
Laura SchreinerDepartment of Pharmacy, Pharmaceutical Biotechnology, University of Munich, Munich, Germany.
Matthias ZornDepartment of Physics, Soft Matter Physics and Biophysics, University of Munich, Munich, Germany.
Florian FoersterDepartment of Pharmacy, Pharmaceutical Biology, University of Munich, Munich, Germany.
Rolf MuellerHelmholtz Institute for Pharmaceutical Research Saarland, Helmholtz Centre for Infection Research and Department of Pharmaceutical Biotechnology, Saarland University, Saarbrücken, Germany.
Joachim O RaedlerDepartment of Physics, Soft Matter Physics and Biophysics, University of Munich, Munich, Germany.
Ernst WagnerDepartment of Pharmacy, Pharmaceutical Biotechnology, University of Munich, Munich, Germany.
Angelika M VollmarDepartment of Pharmacy, Pharmaceutical Biology, University of Munich, Munich, Germany.
Stefan ZahlerDepartment of Pharmacy, Pharmaceutical Biology, University of Munich, Munich, Germany.
Ludwig-Maximilians-Universität München · DESaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA major player in the process of metastasis is the actin cytoskeleton as it forms key structures in both invasion mechanisms, mesenchymal and amoeboid migration. We tested the actin binding compound Chondramide as potential anti-metastatic agent.

methodsIn vivo, the effect of Chondramide on metastasis was tested employing a 4T1-Luc BALB/c mouse model. In vitro, Chondramide was tested using the highly invasive cancer cell line MDA-MB-231 in Boyden-chamber assays, fluorescent stainings, Western blot and Pull down assays. Finally, the contractility of MDA-MB-231 cells was monitored in 3D environment and analyzed via PIV analysis.

resultsIn vivo, Chondramide treatment inhibits metastasis to the lung and the migration and invasion of MDA-MB-231 cells is reduced by Chondramide in vitro. On the signaling level, RhoA activity is decreased by Chondramide accompanied by reduced MLC-2 and the stretch induced guanine nucleotide exchange factor Vav2 activation. At same conditions, EGF-receptor autophosphorylation, Akt and Erk as well as Rac1 are not affected. Finally, Chondramide treatment disrupted the actin cytoskeleton and decreased the ability of cells for contraction.

conclusionsChondramide inhibits cellular contractility and thus represents a potential inhibitor of tumor cell invasion.

Indexed as

Gene Expression Regulation, NeoplasticActin CytoskeletonAnimalsAntineoplastic AgentsBreast NeoplasmsCardiac MyosinsCell Line, TumorCell MovementContractile ProteinsDepsipeptidesFemaleHumansInjections, IntravenousLungLung NeoplasmsMammary Glands, AnimalAntineoplastic AgentsCardiac Myosinschondramide AContractile ProteinsDepsipeptidesmyosin light chain 2Myosin Light ChainsPeptides, CyclicProto-Oncogene Proteins c-vavrhoA GTP-Binding ProteinVav2 protein, mouse

Identifiers

PMID25391145
PMCPMC4229209
OpenAlexW1969962328

What OpenQuestion holds

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LicenceCC BY
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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.