ArticleThe European physical journal. E, Soft matter2022
Actomyosin contractility requirements and reciprocal cell-tissue mechanics for cancer cell invasion through collagen-based channels.
Article in The European physical journal. E, Soft matter, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 20 citations in OpenAlex.
- Adipose-mimetic granular hydrogels uncover biophysical cues driving breast cancer invasion.Cell biomaterials · 2026Article
- Revealing biomechanical vulnerabilities in oral cancer cells using 3D coculture platform and low-frequency ultrasound.Materials today. Bio · 2026Article
- Generation of In Vivo-Inspired 3D Collagen Models for Guided Tumor Invasion In Vitro.Current protocols · 2026Article
- Brillouin Microscopy of Breast tumor Spheroids On-a-Chip: Mechanical and Transcriptional Responses to Microfluidic-Induced Rapid Deformations.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The influence of cell phenotype on collective cell invasion into the extracellular matrix.Bulletin of mathematical biology · 2025Article
- Adipose-mimetic granular hydrogels uncover biophysical cues driving breast cancer invasion.bioRxiv : the preprint server for biology · 2025Article
- Biomechanics of the tumor extracellular matrix and regulatory T cells: regulatory mechanisms and potential therapeutic targets.Cell communication and signaling : CCS · 2025Review
- Leveraging femtosecond laser machining for the fabrication of tubular-based Organ-on-Chip systems: modeling cancer metastasis from invasion to intravasation.Materials today. Bio · 2025Article
- Advances in microfluidic platforms for tumor cell phenotyping: from bench to bedside.Lab on a chip · 2025Review
- Confined cell migration along extracellular matrix space in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Confinement-sensitive volume regulation dynamics via high-speed nuclear morphological measurements.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Extracellular Matrix Components and Mechanosensing Pathways in Health and Disease.Biomolecules · 2024Review
- Tensions on the actin cytoskeleton and apical cell junctions in thebioRxiv : the preprint server for biology · 2024Article
- Microinterfaces in biopolymer-based bicontinuous hydrogels guide rapid 3D cell migration.Nature communications · 2024Article
- Tensions on the actin cytoskeleton and apical cell junctions in theFrontiers in cell and developmental biology · 2024Article
- Cell jamming in a collagen-based interface assay is tuned by collagen density and proteolysis.Journal of cell science · 2023Article
- Uptake of H-ferritin by Glioblastoma stem cells and its impact on their invasion capacity.Journal of cancer research and clinical oncology · 2023Article
- AnFrontiers in bioengineering and biotechnology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The interstitial tumor microenvironment is composed of heterogeneously organized collagen-rich porous networks as well as channel-like structures and interfaces which provide both barriers and guidance for invading cells. Tumor cells invading 3D random porous collagen networks depend upon actomyosin contractility to deform and translocate the nucleus, whereas Rho/Rho-associated kinase-dependent contractility is largely dispensable for migration in stiff capillary-like confining microtracks. To investigate whether this dichotomy of actomyosin contractility dependence also applies to physiological, deformable linear collagen environments, we developed nearly barrier-free collagen-scaffold microtracks of varying cross section using two-photon laser ablation. Both very narrow and wide tracks supported single-cell migration by either outward pushing of collagen up to four times when tracks were narrow, or cell pulling on collagen walls down to 50% of the original diameter by traction forces of up to 40 nN when tracks were wide, resulting in track widths optimized to single-cell diameter. Targeting actomyosin contractility by synthetic inhibitors increased cell elongation and nuclear shape change in narrow tracks and abolished cell-mediated deformation of both wide and narrow tracks. Accordingly, migration speeds in all channel widths reduced, with migration rates of around 45-65% of the original speed persisting. Together, the data suggest that cells engage actomyosin contraction to reciprocally adjust both own morphology and linear track width to optimal size for effective cellular locomotion.
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Registered trials
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.