Evidence map›Paper›PMID 27826898›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2017

Collective cell migration of thyroid carcinoma cells: a beneficial ability to override unfavourable substrates.

Liudmila Lobastova, Dominik Kraus, Alexander Glassmann, Dilaware Khan, Christian Steinhäuser, Christina Wolff, Nadine Veit, Jochen Winter, Rainer Probstmeier

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 15 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

9 authors at 2 institutions in 1 country.

Liudmila LobastovaNeuro- and Tumor Cell Biology Group, Department of Nuclear Medicine, University Hospital Bonn, Sigmund-Freud-Str. 25, D-53105, Bonn, Germany.
Dominik KrausDepartment of Prosthodontics, Preclinical Education, and Material Science, University of Bonn, Bonn, Germany.
Alexander GlassmannLife Science Inkubator, Bonn, Germany.
Dilaware KhanInstitute of Cellular Neurosciences, Medical Faculty, University of Bonn, Bonn, Germany.
Christian SteinhäuserInstitute of Cellular Neurosciences, Medical Faculty, University of Bonn, Bonn, Germany.
Christina WolffNeuro- and Tumor Cell Biology Group, Department of Nuclear Medicine, University Hospital Bonn, Sigmund-Freud-Str. 25, D-53105, Bonn, Germany.
Nadine VeitNeuro- and Tumor Cell Biology Group, Department of Nuclear Medicine, University Hospital Bonn, Sigmund-Freud-Str. 25, D-53105, Bonn, Germany.
Jochen WinterOral Cell Biology Group, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany.
Rainer ProbstmeierNeuro- and Tumor Cell Biology Group, Department of Nuclear Medicine, University Hospital Bonn, Sigmund-Freud-Str. 25, D-53105, Bonn, Germany. r.probstmeier@uni-bonn.de.ORCID http://orcid.org/0000-0001-7671-0373
University Hospital Bonn · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTumor cell invasion and metastasis are life threatening events. Invasive tumor cells tend to migrate as collective sheets. In the present in vitro study we aimed to (i) assess whether collective tumor cells gain benefits in their migratory potential compared to single cells and (ii) to identify its putative underlying molecular mechanisms.

methodsThe migratory potential of single and collective carcinoma cells was assessed using video time lapse microscopy and cell migration assays in the absence and presence of seven potential gap junction inhibitors or the Rac1 inhibitor Z62954982. The perturbation of gap junctions was assessed using a dye diffusion assay. In addition, LDH-based cytotoxicity and RT-PCR-based expression analyses were performed.

resultsWhereas single breast, cervix and thyroid carcinoma cells were virtually immobile on unfavourable plastic surfaces, we found that they gained pronounced migratory capacities as collectives under comparable conditions. Thyroid carcinoma cells, that were studied in more detail, were found to express specific subsets of connexins and to form active gap junctions as revealed by dye diffusion analysis. Although all potential gap junction blockers suppressed intercellular dye diffusion in at least one of the cell lines tested, only two of them were found to inhibit collective cell migration and none of them to inhibit single cell migration. In the presence of the Rac1 inhibitor Z62954982 collective migration, but not single cell migration, was found to be reduced up to 20 %.

conclusionsOur data indicate that collective migration enables tumor cells to cross otherwise unfavourable substrate areas. This capacity seems to be independent of intercellular communication via gap junctions, whereas Rac1-dependent intracellular signalling seems to be essential.

Indexed as

Breast NeoplasmsCell CommunicationCell Line, TumorCell MovementFemaleGap JunctionsHumansNeoplasm Invasivenessrac1 GTP-Binding ProteinReverse Transcriptase Polymerase Chain ReactionSignal TransductionThyroid NeoplasmsUterine Cervical Neoplasmsrac1 GTP-Binding ProteinRAC1 protein, humanCollective cell migrationGap junctionRacSingle cell migrationThyroid carcinoma

Identifiers

PMID27826898
PMCPMC13001555
OpenAlexW2556373981

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.