Evidence map›Paper›PMID 29184140›Full record

ArticleNature communications2017

Induced cortical tension restores functional junctions in adhesion-defective carcinoma cells.

Shoko Ito, Satoru Okuda, Masako Abe, Mari Fujimoto, Tetsuo Onuki, Tamako Nishimura, Masatoshi Takeichi

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 53 citations in OpenAlex.

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  11. Roles of the Dbl family of RhoGEFs in mechanotransduction - a review.Frontiers in cell and developmental biology · 2024
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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 3 institutions in 1 country.

Shoko ItoLaboratory for Cell Adhesion and Tissue Patterning, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-Minamimachi, Chuo-ku, Kobe, 650-0047, Japan.
Satoru OkudaLaboratoty for In Vitro Histogenesis, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-Minamimachi, Chuo-ku, Kobe, 650-0047, Japan.
Masako AbeSeed Compounds Exploratory Unit for Drug Discovery Platform, Drug Discovery Platforms Cooperation Division, RIKEN Center for Sustainable Resource Science, 2-1 Hirosawa, Wako, 351-0198, Japan.
Mari FujimotoSeed Compounds Exploratory Unit for Drug Discovery Platform, Drug Discovery Platforms Cooperation Division, RIKEN Center for Sustainable Resource Science, 2-1 Hirosawa, Wako, 351-0198, Japan.
Tetsuo OnukiSeed Compounds Exploratory Unit for Drug Discovery Platform, Drug Discovery Platforms Cooperation Division, RIKEN Center for Sustainable Resource Science, 2-1 Hirosawa, Wako, 351-0198, Japan.
Tamako NishimuraLaboratory for Cell Adhesion and Tissue Patterning, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-Minamimachi, Chuo-ku, Kobe, 650-0047, Japan.
Masatoshi TakeichiLaboratory for Cell Adhesion and Tissue Patterning, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-Minamimachi, Chuo-ku, Kobe, 650-0047, Japan. takeichi@cdb.riken.jp.ORCID http://orcid.org/0000-0002-9931-3378
RIKEN Center for Sustainable Resource Science · JPRIKEN Center for Computational Science · JPRIKEN Center for Biosystems Dynamics Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Normal epithelial cells are stably connected to each other via the apical junctional complex (AJC). AJCs, however, tend to be disrupted during tumor progression, and this process is implicated in cancer dissemination. Here, using colon carcinoma cells that fail to form AJCs, we investigated molecular defects behind this failure through a search for chemical compounds that could restore AJCs, and found that microtubule-polymerization inhibitors (MTIs) were effective. MTIs activated GEF-H1/RhoA signaling, causing actomyosin contraction at the apical cortex. This contraction transmitted force to the cadherin-catenin complex, resulting in a mechanosensitive recruitment of vinculin to cell junctions. This process, in turn, recruited PDZ-RhoGEF to the junctions, leading to the RhoA/ROCK/LIM kinase/cofilin-dependent stabilization of the junctions. RhoGAP depletion mimicked these MTI-mediated processes. Cells that normally organize AJCs did not show such MTI/RhoA sensitivity. Thus, advanced carcinoma cells require elevated RhoA activity for establishing robust junctions, which triggers tension-sensitive reorganization of actin/adhesion regulators.

Indexed as

Actin CytoskeletonActin Depolymerizing FactorsActinsActomyosinAdherens JunctionsBiomechanical PhenomenaCaco-2 CellsCadherinsCell AdhesionCell Adhesion MoleculesCell Line, TumorColonic NeoplasmsCytoskeletal ProteinsEpithelial CellsGuanine Nucleotide Exchange FactorsHT29 CellsActin Depolymerizing FactorsActinsActomyosinCadherinsCell Adhesion MoleculesCytoskeletal ProteinsGuanine Nucleotide Exchange FactorsLIMK1 protein, humanLim KinasesMyosin Type IINocodazolerhoA GTP-Binding Proteinrho-Associated KinasesVCL protein, humanVinculin

Identifiers

PMID29184140
PMCPMC5705652
OpenAlexW2770421887

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.