Evidence map›Paper›PMID 31659296›Full record

ArticleNature materials2020

Stopping transformed cancer cell growth by rigidity sensing.

Bo Yang, Haguy Wolfenson, Vin Yee Chung, Naotaka Nakazawa, Shuaimin Liu, Junqiang Hu, Ruby Yun-Ju Huang, Michael P Sheetz

Open access · greenAbstract read
In one paragraph

Article in Nature materials, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
8.2field-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

64 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Mechanomedicine.Nature reviews bioengineering · 2026
    Article
  6. Article
  7. Article
  8. Nuclear destabilisation - a possible genesis of cancer?Biological reviews of the Cambridge Philosophical Society · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 4 countries.

Bo YangMechanobiology Institute, National University of Singapore, Singapore, Singapore.
Haguy WolfensonDepartment of Genetics and Developmental Biology, The Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel of Technology, Haifa, Israel.ORCID http://orcid.org/0000-0001-6892-7839
Vin Yee ChungCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Naotaka NakazawaMechanobiology Institute, National University of Singapore, Singapore, Singapore.ORCID http://orcid.org/0000-0002-8695-4344
Shuaimin LiuDepartment of Mechanical Engineering, Columbia University, New York, NY, USA.
Junqiang HuDepartment of Mechanical Engineering, Columbia University, New York, NY, USA.
Ruby Yun-Ju HuangCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Michael P SheetzMechanobiology Institute, National University of Singapore, Singapore, Singapore. ms2001@columbia.edu.ORCID http://orcid.org/0000-0001-8747-3430
National University of Singapore · SGColumbia University · USTechnion – Israel Institute of Technology · IL

Funding

Tropomyosin and tyrosine kinases in mechanics of cancerR01GM113022 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SHEETZ, MICHAEL PATRICK · 2015 to 2018
$1.2M
NIGMS NIH HHS R01 GM113022
6 · The paper itself

Abstract

A common feature of cancer cells is the alteration of kinases and biochemical signalling pathways enabling transformed growth on soft matrices, whereas cytoskeletal protein alterations are thought to be a secondary issue. However, we report here that cancer cells from different tissues can be toggled between transformed and rigidity-dependent growth states by the absence or presence of mechanosensory modules, respectively. In various cancer lines from different tissues, cells had over tenfold fewer rigidity-sensing contractions compared with normal cells from the same tissues. Restoring normal levels of cytoskeletal proteins, including tropomyosins, restored rigidity sensing and rigidity-dependent growth. Further depletion of other rigidity sensor proteins, including myosin IIA, restored transformed growth and blocked sensing. In addition, restoration of rigidity sensing to cancer cells inhibited tumour formation and changed expression patterns. Thus, the depletion of rigidity-sensing modules through alterations in cytoskeletal protein levels enables cancer cell growth on soft surfaces, which is an enabling factor for cancer progression.

Indexed as

Cell Transformation, NeoplasticMechanical PhenomenaBiomechanical PhenomenaCell Line, TumorCell ProliferationCytoskeletal ProteinsFibroblastsHumansTropomyosinCytoskeletal ProteinsTPM3 protein, humanTropomyosin

Identifiers

PMID31659296
PMCPMC7477912
OpenAlexW2982144197

What OpenQuestion holds

Textmetadata
LicenceTDM
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.