Evidence map›Paper›PMID 39372730›Full record

ArticlebioRxiv : the preprint server for biology2024

Restoring mechanophenotype reverts malignant properties of ECM-enriched vocal fold cancer.

Jasmin Kaivola, Karolina Punovuori, Megan R Chastney, Yekaterina A Miroshnikova, Hind Abdo, Fabien Bertillot, Fabian Krautgasser, Jasmin Di Franco, James R W Conway, Gautier Follain and 9 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Jasmin KaivolaTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.
Karolina PunovuoriStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki Finland.ORCID 0000-0003-0297-1225
Megan R ChastneyTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.
Yekaterina A MiroshnikovaStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki Finland.
Hind AbdoIFOM, the FIRC Institute of Molecular Oncology, Milan, Italy.
Fabien BertillotStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki Finland.
Fabian KrautgasserFaculty of Physics, University of Vienna, Vienna, Austria.
Jasmin Di FrancoFaculty of Physics, University of Vienna, Vienna, Austria.
James R W ConwayTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.ORCID 0000-0003-3787-277X
Gautier FollainTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.
Jaana HagströmInstitute for Molecular Medicine Finland, Helsinki Institute of Life Science, University of Helsinki, Helsinki, Finland.
Antti MäkitieDepartment of Otorhinolaryngology - Head and Neck Surgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Heikki IrjalaDepartment of Otorhinolaryngology-Head and Neck Surgery, University of Turku and Turku University Hospital, Turku, Finland.
Sami VenteläTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.
Hellyeh HamidiTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.
Giorgio ScitaDepartment of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0001-7984-1889
Roberto CerbinoFaculty of Physics, University of Vienna, Vienna, Austria.
Sara A WickströmStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki Finland.
Johanna IvaskaTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.ORCID 0000-0002-6295-6556

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased extracellular matrix (ECM) and matrix stiffness promote solid tumor progression. However, mechanotransduction in cancers arising in mechanically active tissues remains underexplored. Here, we report upregulation of multiple ECM components accompanied by tissue stiffening in vocal fold cancer (VFC). We compare non-cancerous (NC) and patient-derived VFC cells - from early (mobile, T1) to advanced-stage (immobile, T3) cancers - revealing an association between VFC progression and cell-surface receptor heterogeneity, reduced laminin-binding integrin cell-cell junction localization and a flocking mode of collective cell motility. Mimicking physiological movement of healthy vocal fold tissue (stretching/vibration), decreases oncogenic nuclear β-catenin and YAP levels in VFC. Multiplex immunohistochemistry of VFC tumors uncovered a correlation between ECM content, nuclear YAP and patient survival, concordant with VFC sensitivity to YAP-TEAD inhibitors in vitro. Our findings present evidence that VFC is a mechanically sensitive malignancy and restoration of tumor mechanophenotype or YAP/TAZ targeting, represents a tractable anti-oncogenic therapeutic avenue for VFC.

Identifiers

PMID39372730
PMCPMC11451600

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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.