Evidence map›Paper›PMID 33082491›Full record

ArticleCommunications biology2020

Effects of energy metabolism on the mechanical properties of breast cancer cells.

Marina L Yubero, Priscila M Kosaka, Álvaro San Paulo, Marcos Malumbres, Montserrat Calleja, Javier Tamayo

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 41 citations in OpenAlex.

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  3. High-Throughput Nanorheology of Living Cells Powered by Supervised Machine Learning.Advanced intelligent systems (Weinheim an der Bergstrasse, Germany) · 2025
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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

6 authors at 2 institutions in 1 country.

Marina L YuberoBionanomechanics Lab, Instituto de Micro y Nanotecnología, IMN-CNM (CSIC), Isaac Newton 8 (PTM), E-28760, Tres Cantos, Madrid, Spain.ORCID 0000-0003-3751-4702
Priscila M KosakaBionanomechanics Lab, Instituto de Micro y Nanotecnología, IMN-CNM (CSIC), Isaac Newton 8 (PTM), E-28760, Tres Cantos, Madrid, Spain.ORCID 0000-0003-4242-7064
Álvaro San PauloBionanomechanics Lab, Instituto de Micro y Nanotecnología, IMN-CNM (CSIC), Isaac Newton 8 (PTM), E-28760, Tres Cantos, Madrid, Spain.
Marcos MalumbresCell Division and Cancer Group, Centro Nacional de Investigaciones Oncológicas (CNIO), C/ Melchor Fernández Almagro, 3, E-28029, Madrid, Spain.
Montserrat CallejaBionanomechanics Lab, Instituto de Micro y Nanotecnología, IMN-CNM (CSIC), Isaac Newton 8 (PTM), E-28760, Tres Cantos, Madrid, Spain.ORCID 0000-0003-2414-5725
Javier TamayoBionanomechanics Lab, Instituto de Micro y Nanotecnología, IMN-CNM (CSIC), Isaac Newton 8 (PTM), E-28760, Tres Cantos, Madrid, Spain. jtamayo@imm.cnm.csic.es.ORCID 0000-0002-5280-7215
Institute of Micro and Nanotechnology · ESSpanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumorigenesis induces actin cortex remodeling, which makes cancerous cells softer. Cell deformability is largely determined by myosin-driven cortical tension and actin fiber architecture at the cell cortex. However, it is still unclear what the weight of each contribution is, and how these contributions change during cancer development. Moreover, little attention has been paid to the effect of energy metabolism on this phenomenon and its reprogramming in cancer. Here, we perform precise two-dimensional mechanical phenotyping based on power-law rheology to unveil the contributions of myosin II, actin fiber architecture and energy metabolism to the deformability of healthy (MCF-10A), noninvasive cancerous (MCF-7), and metastatic (MDA-MB-231) human breast epithelial cells. Contrary to the perception that the actin cortex is a passive structure that provides mechanical resistance to the cell, we find that this is only true when the actin cortex is activated by metabolic processes. The results show marked differences in the nature of the active processes that build up cell stiffness, namely that healthy cells use ATP-driven actin polymerization whereas metastatic cells use myosin II activity. Noninvasive cancerous cells exhibit an anomalous behavior, as their stiffness is not as affected by the lack of nutrients and ATP, suggesting that energy metabolism reprogramming is used to sustain active processes at the actin cortex.

Indexed as

Energy MetabolismMechanical PhenomenaModels, TheoreticalActinsAdenosine TriphosphateBiomarkersBiophysical PhenomenaBreast NeoplasmsCell Transformation, NeoplasticCytoskeletonElasticityFemaleHumansMicroscopy, Atomic ForceMyosin Type IINeoplasm InvasivenessActinsAdenosine TriphosphateBiomarkersMyosin Type II

Identifiers

PMID33082491
PMCPMC7576174
OpenAlexW3094052369

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.