Evidence map›Paper›PMID 30113874›Full record

ArticleMolecular biology of the cell2018

Cell cycle-dependent force transmission in cancer cells.

Magdalini Panagiotakopoulou, Tobias Lendenmann, Francesca Michela Pramotton, Costanza Giampietro, Georgios Stefopoulos, Dimos Poulikakos, Aldo Ferrari

Erratum issuedAbstract read
In one paragraph

Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Magdalini PanagiotakopoulouLaboratory of Thermodynamics in Emerging Technologies, Department of Mechanical and Process Engineering, ETH Zurich, CH-8092 Zürich, Switzerland.
Tobias LendenmannLaboratory of Thermodynamics in Emerging Technologies, Department of Mechanical and Process Engineering, ETH Zurich, CH-8092 Zürich, Switzerland.
Francesca Michela PramottonLaboratory of Thermodynamics in Emerging Technologies, Department of Mechanical and Process Engineering, ETH Zurich, CH-8092 Zürich, Switzerland.
Costanza GiampietroLaboratory of Thermodynamics in Emerging Technologies, Department of Mechanical and Process Engineering, ETH Zurich, CH-8092 Zürich, Switzerland.
Georgios StefopoulosLaboratory of Thermodynamics in Emerging Technologies, Department of Mechanical and Process Engineering, ETH Zurich, CH-8092 Zürich, Switzerland.
Dimos PoulikakosLaboratory of Thermodynamics in Emerging Technologies, Department of Mechanical and Process Engineering, ETH Zurich, CH-8092 Zürich, Switzerland.
Aldo FerrariLaboratory of Thermodynamics in Emerging Technologies, Department of Mechanical and Process Engineering, ETH Zurich, CH-8092 Zürich, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The generation of traction forces and their transmission to the extracellular environment supports the disseminative migration of cells from a primary tumor. In cancer cells, the periodic variation of nuclear stiffness during the cell cycle provides a functional link between efficient translocation and proliferation. However, the mechanical framework completing this picture remains unexplored. Here, the Fucci2 reporter was expressed in various human epithelial cancer cells to resolve their cell cycle phase transition. The corresponding tractions were captured by a recently developed reference-free confocal traction-force microscopy platform. The combined approach was conducive to the analysis of phase-dependent force variation at the level of individual integrin contacts. Detected forces were invariably higher in the G1 and early S phases than in the ensuing late S/G2, and locally colocalized with high levels of paxillin phosphorylation. Perturbation of paxillin phosphorylation at focal adhesions, obtained through the biochemical inhibition of focal adhesion kinase (FAK) or the transfection of nonphosphorylatable or phosphomimetic paxillin mutants, significantly diminished the force transmitted to the substrate. These data demonstrate a reproducible modulation of force transmission during the cell cycle progression of cancer cells, instrumental to their invasion of dense environments. In addition, they delineate a model in which paxillin phosphorylation supports the mechanical maturation of adhesions relaying forces to the substrate.

Indexed as

Cell CycleBiomechanical PhenomenaCell MovementCell ProliferationDrug Resistance, NeoplasmFocal Adhesion Protein-Tyrosine KinasesHEK293 CellsHeLa CellsHumansMCF-7 CellsNeoplasm InvasivenessNeoplasmsPaxillinPhenotypePhosphorylationTamoxifenFocal Adhesion Protein-Tyrosine KinasesPaxillinTamoxifen

Identifiers

PMID30113874
PMCPMC6254576

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.