Evidence map›Paper›PMID 34635648›Full record

ArticleNature communications2021

Homeostatic membrane tension constrains cancer cell dissemination by counteracting BAR protein assembly.

Kazuya Tsujita, Reiko Satow, Shinobu Asada, Yoshikazu Nakamura, Luis Arnes, Keisuke Sako, Yasuyuki Fujita, Kiyoko Fukami, Toshiki Itoh

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 92 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Ether lipids influence cancer cell fate by modulating iron uptake.bioRxiv : the preprint server for biology · 2025
    Article
  8. Hypoxia Modulates Membrane Mechanics in Pancreatic Cancer.The Journal of membrane biology · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Focus on mechano-immunology: new direction in cancer treatment.International journal of surgery (London, England) · 2025
    Review
  18. Article
  19. Article
  20. Review
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

9 authors at 6 institutions in 2 countries.

Kazuya TsujitaBiosignal Research Center, Kobe University, Kobe, Hyogo, 657-8501, Japan. tsujita@people.kobe-u.ac.jp.ORCID 0000-0002-1860-6831
Reiko SatowLaboratory of Genome and Biosignals, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Shinobu AsadaLaboratory of Genome and Biosignals, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Yoshikazu NakamuraLaboratory of Genome and Biosignals, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Luis ArnesThe Novo Nordisk Foundation Center for Stem Cell Biology (DanStem), Biotech Research & Innovation Centre, University of Copenhagen, Copenhagen, Denmark.
Keisuke SakoNational Cerebral and Cardiovascular Center Research Institute, Osaka, 565-8565, Japan.ORCID 0000-0002-6453-8075
Yasuyuki FujitaDivision of Molecular Oncology, Graduate School of Medicine, Kyoto University, Kyoto, 606-8501, Japan.
Kiyoko FukamiLaboratory of Genome and Biosignals, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Toshiki ItohBiosignal Research Center, Kobe University, Kobe, Hyogo, 657-8501, Japan.
Tokyo University of Pharmacy and Life Sciences · JPJapan Agency for Medical Research and Development · JPKobe University · JPKyoto University · JPNational Cerebral and Cardiovascular Center · JPUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignancy is associated with changes in cell mechanics that contribute to extensive cell deformation required for metastatic dissemination. We hypothesized that the cell-intrinsic physical factors that maintain epithelial cell mechanics could function as tumor suppressors. Here we show, using optical tweezers, genetic interference, mechanical perturbations, and in vivo studies, that epithelial cells maintain higher plasma membrane (PM) tension than their metastatic counterparts and that high PM tension potently inhibits cancer cell migration and invasion by counteracting membrane curvature sensing/generating BAR family proteins. This tensional homeostasis is achieved by membrane-to-cortex attachment (MCA) regulated by ERM proteins, whose disruption spontaneously transforms epithelial cells into a mesenchymal migratory phenotype powered by BAR proteins. Consistently, the forced expression of epithelial-mesenchymal transition (EMT)-inducing transcription factors results in decreased PM tension. In metastatic cells, increasing PM tension by manipulating MCA is sufficient to suppress both mesenchymal and amoeboid 3D migration, tumor invasion, and metastasis by compromising membrane-mediated mechanosignaling by BAR proteins, thereby uncovering a previously undescribed mechanical tumor suppressor mechanism.

Indexed as

Biomechanical PhenomenaCell Line, TumorCell MembraneCell MovementDNA-Binding ProteinsEpithelial CellsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHippo KinasesHomeostasisHumansLymphatic MetastasisMechanotransduction, CellularNeoplasm InvasivenessOptical TweezersProtein Serine-Threonine KinasesDNA-Binding ProteinsETV5 protein, humanHippo KinasesProtein Serine-Threonine KinasesrhoA GTP-Binding ProteinRHOA protein, humanSLK protein, humanTranscription Factors

Identifiers

PMID34635648
PMCPMC8505629
OpenAlexW3205833934

What Socratic 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 Socratic graph.