Evidence map›Paper›PMID 38637494›Full record

ArticleNature communications2024

Membrane to cortex attachment determines different mechanical phenotypes in LGR5+ and LGR5- colorectal cancer cells.

Sefora Conti, Valeria Venturini, Adrià Cañellas-Socias, Carme Cortina, Juan F Abenza, Camille Stephan-Otto Attolini, Emily Middendorp Guerra, Catherine K Xu, Jia Hui Li, Leone Rossetti and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
8.2field-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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  7. Collective migration modes in development, tissue repair and cancer.Nature reviews. Molecular cell biology · 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

18 authors at 7 institutions in 3 countries.

Sefora ContiInstitute for Bioengineering of Catalonia (IBEC), The Barcelona Institute for Science and Technology (BIST), Barcelona, Spain.
Valeria VenturiniCentre for Genomic Regulation (CRG), The Barcelona Institute for Science and Technology (BIST), Barcelona, Spain.ORCID http://orcid.org/0000-0003-2526-6473
Adrià Cañellas-SociasInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID http://orcid.org/0000-0002-8373-7803
Carme CortinaInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Juan F AbenzaInstitute for Bioengineering of Catalonia (IBEC), The Barcelona Institute for Science and Technology (BIST), Barcelona, Spain.
Camille Stephan-Otto AttoliniInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID http://orcid.org/0000-0001-8045-320X
Emily Middendorp GuerraInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Catherine K XuMax Planck Institute for the Science of Light, Erlangen, Germany.ORCID http://orcid.org/0000-0003-4726-636X
Jia Hui LiCell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
Leone RossettiInstitute for Bioengineering of Catalonia (IBEC), The Barcelona Institute for Science and Technology (BIST), Barcelona, Spain.
Giorgio StassiDepartment of Surgical Oncological and Stomatological Sciences, University of Palermo, Palermo, Italy.ORCID http://orcid.org/0000-0002-1016-9059
Pere Roca-CusachsInstitute for Bioengineering of Catalonia (IBEC), The Barcelona Institute for Science and Technology (BIST), Barcelona, Spain.ORCID http://orcid.org/0000-0001-6947-961X
Alba Diz-MuñozCell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
Verena RuprechtCentre for Genomic Regulation (CRG), The Barcelona Institute for Science and Technology (BIST), Barcelona, Spain.ORCID http://orcid.org/0000-0003-4088-8633
Jochen GuckMax Planck Institute for the Science of Light, Erlangen, Germany.ORCID http://orcid.org/0000-0002-1453-6119
Eduard BatlleInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. eduard.batlle@irbbarcelona.org.ORCID http://orcid.org/0000-0003-2422-0326
Anna LabernadieInstitute for Bioengineering of Catalonia (IBEC), The Barcelona Institute for Science and Technology (BIST), Barcelona, Spain. alabernadie@cipf.es.ORCID http://orcid.org/0000-0001-5768-5088
Xavier TrepatInstitute for Bioengineering of Catalonia (IBEC), The Barcelona Institute for Science and Technology (BIST), Barcelona, Spain. xtrepat@ibecbarcelona.eu.ORCID http://orcid.org/0000-0002-7621-5214
Barcelona Institute of Science and Technology · ESInstitute for Research in Biomedicine · ESInstitució Catalana de Recerca i Estudis Avançats · ESEuropean Molecular Biology Laboratory · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEMax Planck Institute for the Science of Light · DEUniversity of Palermo · IT

Funding

EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) Adv-883739
6 · The paper itself

Abstract

Colorectal cancer (CRC) tumors are composed of heterogeneous and plastic cell populations, including a pool of cancer stem cells that express LGR5. Whether these distinct cell populations display different mechanical properties, and how these properties might contribute to metastasis is poorly understood. Using CRC patient derived organoids (PDOs), we find that compared to LGR5- cells, LGR5+ cancer stem cells are stiffer, adhere better to the extracellular matrix (ECM), move slower both as single cells and clusters, display higher nuclear YAP, show a higher survival rate in response to mechanical confinement, and form larger transendothelial gaps. These differences are largely explained by the downregulation of the membrane to cortex attachment proteins Ezrin/Radixin/Moesin (ERMs) in the LGR5+ cells. By analyzing single cell RNA-sequencing (scRNA-seq) expression patterns from a patient cohort, we show that this downregulation is a robust signature of colorectal tumors. Our results show that LGR5- cells display a mechanically dynamic phenotype suitable for dissemination from the primary tumor whereas LGR5+ cells display a mechanically stable and resilient phenotype suitable for extravasation and metastatic growth.

Indexed as

Colorectal NeoplasmsReceptors, G-Protein-CoupledHumansNeoplastic Stem CellsPhenotypeLGR5 protein, humanReceptors, G-Protein-Coupled

Identifiers

PMID38637494
PMCPMC11026456
OpenAlexW4394908834

What OpenQuestion holds

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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.