Evidence map›Paper›PMID 32187555›Full record

ArticleCell reports2020

Cancer Cells Resist Mechanical Destruction in Circulation via RhoA/Actomyosin-Dependent Mechano-Adaptation.

Devon L Moose, Benjamin L Krog, Tae-Hyung Kim, Lei Zhao, Sophia Williams-Perez, Gretchen Burke, Lillian Rhodes, Marion Vanneste, Patrick Breheny, Mohammed Milhem and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing 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

78 citing papers in PubMed, 104 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Model Circulating Tumor Cells Induced by Mechanical Stress.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

18 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

13 authors at 3 institutions in 1 country.

Devon L MooseDepartment of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA; Cancer Biology Program, Biomedical Sciences, University of Iowa, Iowa City, IA 52242, USA.
Benjamin L KrogDepartment of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA; Department of Biomedical Engineering, College of Engineering, University of Iowa, Iowa City, IA 52242, USA.
Tae-Hyung KimDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Lei ZhaoDepartment of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Sophia Williams-PerezCarver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Gretchen BurkeDepartment of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Lillian RhodesDepartment of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Marion VannesteDepartment of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Patrick BrehenyDepartment of Biostatistics, College of Public Health, University of Iowa, Iowa City, IA 52242, USA.
Mohammed MilhemHolden Comprehensive Cancer Center, Iowa City, IA 52242, USA; Division of Hematology and Oncology, Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Christopher S StippDepartment of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA; Holden Comprehensive Cancer Center, Iowa City, IA 52242, USA; Department of Biology, University of Iowa, Iowa City, IA 52242, USA.
Amy C RowatDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Michael D HenryDepartment of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA; Cancer Biology Program, Biomedical Sciences, University of Iowa, Iowa City, IA 52242, USA; Holden Comprehensive Cancer Center, Iowa City, IA 52242, USA; Departments of Pathology, Urology and Radiation Oncology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. Electronic address: michael-henry@uiowa.edu.
University of Iowa · USUniversity of California, Los Angeles · USUniversity of Iowa Holden Comprehensive Cancer Center

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Christopher K Laubenthal · 2000 to 2026
$70.0M
Project 4: New Approaches to Improving the Effectiveness of Radionuclide Targeted Treatments in Neuroendocrine TumorsP50CA174521 · NCI · UNIVERSITY OF IOWA · PI ODORISIO, THOMAS · 2015 to 2021
$13.2M
Predoctoral Training in the Pharmacological SciencesT32GM067795 · NIGMS · UNIVERSITY OF IOWA · PI STRACK, STEFAN · 2004 to 2021
$3.4M
Effects of fluid shear stress on circulating tumor cellsR21CA196202 · NCI · UNIVERSITY OF IOWA · PI HENRY, MICHAEL D · 2016 to 2017
$364k
(PQC2) Resistance to fluid shear stress: a novel biomarker of cancer cellsR21CA179981 · NCI · UNIVERSITY OF IOWA · PI HENRY, MICHAEL D · 2013 to 2014
$356k
NCI NIH HHS P30 CA086862NCI NIH HHS P50 CA174521NCI NIH HHS R21 CA179981NCI NIH HHS R21 CA196202NIGMS NIH HHS T32 GM067795
6 · The paper itself

Abstract

During metastasis, cancer cells are exposed to potentially destructive hemodynamic forces including fluid shear stress (FSS) while en route to distant sites. However, prior work indicates that cancer cells are more resistant to brief pulses of high-level FSS in vitro relative to non-transformed epithelial cells. Herein, we identify a mechano-adaptive mechanism of FSS resistance in cancer cells. Our findings demonstrate that cancer cells activate RhoA in response to FSS, which protects them from FSS-induced plasma membrane damage. We show that cancer cells freshly isolated from mouse and human tumors are resistant to FSS, that formin and myosin II activity protects circulating tumor cells (CTCs) from destruction, and that short-term inhibition of myosin II delays metastasis in mouse models. Collectively, our data indicate that viable CTCs actively resist destruction by hemodynamic forces and are likely to be more mechanically robust than is commonly thought.

Indexed as

Adaptation, BiologicalStress, MechanicalActomyosinAnimalsCell Line, TumorCell MembraneCell SurvivalHemodynamicsHumansMice, Inbred C57BLMyosin Type IINeoplasm MetastasisNeoplasmsNeoplastic Cells, CirculatingrhoA GTP-Binding ProteinShear StrengthActomyosinMyosin Type IIrhoA GTP-Binding ProteinRHOA protein, humancirculating tumor cellsfluid shear stressforminmetastasismyosin IIRhoA

Identifiers

PMID32187555
PMCPMC7219793
OpenAlexW3011226021

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.