Evidence map›Paper›PMID 26189182›Full record

ArticleOncotarget2015

Mechanical phenotype of cancer cells: cell softening and loss of stiffness sensing.

Hsi-Hui Lin, Hsiu-Kuan Lin, I-Hsuan Lin, Yu-Wei Chiou, Horn-Wei Chen, Ching-Yi Liu, Hans I-Chen Harn, Wen-Tai Chiu, Yang-Kao Wang, Meng-Ru Shen and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

88 citing papers in PubMed, 186 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Nuclear destabilisation - a possible genesis of cancer?Biological reviews of the Cambridge Philosophical Society · 2025
    Review
  10. Physical traits of supercompetitors in cell competition.Journal of the Royal Society, Interface · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

28 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

11 authors at 1 institution in 1 country.

Hsi-Hui LinDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Hsiu-Kuan LinInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
I-Hsuan LinDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Yu-Wei ChiouDepartment of Biomedical Engineering, National Cheng Kung University, Tainan, Taiwan.
Horn-Wei ChenDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Ching-Yi LiuInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
Hans I-Chen HarnInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
Wen-Tai ChiuDepartment of Biomedical Engineering, National Cheng Kung University, Tainan, Taiwan.
Yang-Kao WangDepartment of Cell Biology and Anatomy, National Cheng Kung University, Tainan, Taiwan.
Meng-Ru ShenDepartment of Pharmacology, National Cheng Kung University, Tainan, Taiwan.
Ming-Jer TangDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
National Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we determined whether normal cells and cancer cells display distinct mechanical phenotypes. Cancer cells were softer than their normal counterparts, regardless of the type of cancer (breast, bladder, cervix, pancreas, or Ha-RasV12-transformed cells). When cultured on matrices of varying stiffness, low stiffness decreased proliferation in normal cells, while cancer cells and transformed cells lost this response. Thus, cancer cells undergo a change in their mechanical phenotype that includes cell softening and loss of stiffness sensing. Caveolin-1, which is suppressed in many tumor cells and in oncogene-transformed cells, regulates the mechanical phenotype. Caveolin-1-upregulated RhoA activity and Y397FAK phosphorylation directed actin cap formation, which was positively correlated with cell elasticity and stiffness sensing in fibroblasts. Ha-RasV12-induced transformation and changes in the mechanical phenotypes were reversed by re-expression of caveolin-1 and mimicked by the suppression of caveolin-1 in normal fibroblasts. This is the first study to describe this novel role for caveolin-1, linking mechanical phenotype to cell transformation. Furthermore, mechanical characteristics may serve as biomarkers for cell transformation.

Indexed as

ActinsAnimalsBiomechanical PhenomenaCaveolin 1Cell ProliferationCell Transformation, NeoplasticCollagenDogsElasticityEnzyme InhibitorsFemaleFibroblastsGenes, rasHumansMadin Darby Canine Kidney CellsMiceActinsCAV1 protein, humanCaveolin 1CollagenEnzyme Inhibitorsras ProteinsrhoA GTP-Binding ProteinRHOA protein, humancaveolin-1cell stiffnessmatrix stiffnessmechanical phenotypestiffness sensing

Identifiers

PMID26189182
PMCPMC4673241
OpenAlexW1573636649

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.