ArticleCell reports2021
Recursive feedback between matrix dissipation and chemo-mechanical signaling drives oscillatory growth of cancer cell invadopodia.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- EMT and cell cycle control invadopodia and metastasis in breast cancer via Filip1L.Research square · 2026Article
- Mechanical Signaling: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- The role of non-linear viscoelastic hydrogel mechanics in cell culture and transduction.Materials today. Bio · 2025Review
- Regulation of cell migration by extracellular matrix mechanics at a glance.Journal of cell science · 2025Review
- Hydrogel Elastic Energy: A Stressor Triggering an Adaptive Stress-Mediated Cell Response.Advanced healthcare materials · 2025Article
- Cell-extracellular matrix mechanotransduction in 3D.Nature reviews. Molecular cell biology · 2023Review
- Lose the stress: Viscoelastic materials for cell engineering.Acta biomaterialia · 2023Review
- Chemo-mechanical diffusion waves explain collective dynamics of immune cell podosomes.Nature communications · 2023Article
- Predicting YAP/TAZ nuclear translocation in response to ECM mechanosensing.Biophysical journal · 2023Article
- Proteolytic and mechanical remodeling of the extracellular matrix by invadopodia in cancer.Physical biology · 2022Review
- Cell-3D matrix interactions: recent advances and opportunities.Trends in cell biology · 2022Review
- The Elephant in the Cell: Nuclear Mechanics and Mechanobiology.Journal of biomechanical engineering · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Most extracellular matrices (ECMs) are known to be dissipative, exhibiting viscoelastic and often plastic behaviors. However, the influence of dissipation, in particular mechanical plasticity in 3D confining microenvironments, on cell motility is not clear. In this study, we develop a chemo-mechanical model for dynamics of invadopodia, the protrusive structures that cancer cells use to facilitate invasion, by considering myosin recruitment, actin polymerization, matrix deformation, and mechano-sensitive signaling pathways. We demonstrate that matrix dissipation facilitates invadopodia growth by softening ECMs over repeated cycles, during which plastic deformation accumulates via cyclic ratcheting. Our model reveals that distinct protrusion patterns, oscillatory or monotonic, emerge from the interplay of timescales for polymerization-associated extension and myosin recruitment dynamics. Our model predicts the changes in invadopodia dynamics upon inhibition of myosin, adhesions, and the Rho-Rho-associated kinase (ROCK) pathway. Altogether, our work highlights the role of matrix plasticity in invadopodia dynamics and can help design dissipative biomaterials to modulate cancer cell motility.
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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.