Evidence map›Paper›PMID 29467174›Full record

ReviewThe Journal of cell biology2018

Mechanotransduction in tumor progression: The dark side of the force.

Florence Broders-Bondon, Thanh Huong Nguyen Ho-Bouldoires, Maria-Elena Fernandez-Sanchez, Emmanuel Farge

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 1 pooled it
16.7field-weighted citation impact, top 1% 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

175 citing papers in PubMed, 1 synthesis or guideline pooled it, 320 citations in OpenAlex.

  1. Pooled it
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  15. Metal Ions Within the Neuro-Immune-Tumor Axis.Journal of immunology research · 2026
    Review
  16. Review
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  20. Nuclear destabilisation - a possible genesis of cancer?Biological reviews of the Cambridge Philosophical Society · 2025
    Review

115 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Florence Broders-BondonMechanics and Genetics of Embryonic and Tumor Development Group, Institut Curie, PSL Research University, Centre National de la Recherche Scientifique, UMR168, Inserm, Sorbonne Universities, Paris, France.ORCID 0000-0003-3498-0062
Thanh Huong Nguyen Ho-BouldoiresMechanics and Genetics of Embryonic and Tumor Development Group, Institut Curie, PSL Research University, Centre National de la Recherche Scientifique, UMR168, Inserm, Sorbonne Universities, Paris, France.
Maria-Elena Fernandez-SanchezMechanics and Genetics of Embryonic and Tumor Development Group, Institut Curie, PSL Research University, Centre National de la Recherche Scientifique, UMR168, Inserm, Sorbonne Universities, Paris, France.
Emmanuel FargeMechanics and Genetics of Embryonic and Tumor Development Group, Institut Curie, PSL Research University, Centre National de la Recherche Scientifique, UMR168, Inserm, Sorbonne Universities, Paris, France efarge@curie.fr.ORCID 0000-0002-5063-7179
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer has been characterized as a genetic disease, associated with mutations that cause pathological alterations of the cell cycle, adhesion, or invasive motility. Recently, the importance of the anomalous mechanical properties of tumor tissues, which activate tumorigenic biochemical pathways, has become apparent. This mechanical induction in tumors appears to consist of the destabilization of adult tissue homeostasis as a result of the reactivation of embryonic developmental mechanosensitive pathways in response to pathological mechanical strains. These strains occur in many forms, for example, hypervascularization in late tumors leads to high static hydrodynamic pressure that can promote malignant progression through hypoxia or anomalous interstitial liquid and blood flow. The high stiffness of tumors directly induces the mechanical activation of biochemical pathways enhancing the cell cycle, epithelial-mesenchymal transition, and cell motility. Furthermore, increases in solid-stress pressure associated with cell hyperproliferation activate tumorigenic pathways in the healthy epithelial cells compressed by the neighboring tumor. The underlying molecular mechanisms of the translation of a mechanical signal into a tumor inducing biochemical signal are based on mechanically induced protein conformational changes that activate classical tumorigenic signaling pathways. Understanding these mechanisms will be important for the development of innovative treatments to target such mechanical anomalies in cancer.

Indexed as

Disease ProgressionMechanotransduction, CellularAnimalsCarcinogenesisExtracellular MatrixHumansModels, BiologicalNeoplasms

Identifiers

PMID29467174
PMCPMC5940296
OpenAlexW2789065958

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.