ArticleAmerican journal of physiology. Cell physiology2015
Comparative mechanisms of cancer cell migration through 3D matrix and physiological microtracks.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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61 citing papers in PubMed, 103 citations in OpenAlex.
- Amoeboid-mesenchymal transition and the proteolytic control of cancer invasion plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Is there a link between fascia and cancer? From potential mechanisms to future treatment options.Frontiers in physiology · 2026Review
- Measurement of cellular traction forces during confined migration.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Tumor-Tissue Boundaries as Instructive Interfaces in Breast Cancer Cell Invasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Suppression of cofilin-1 promotes invasion in 3D hyaluronic acid matrices by promoting actin-based protrusions.Molecular biology of the cell · 2025Article
- Monocytes use protrusive forces to generate migration paths in viscoelastic collagen-based extracellular matrices.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Regulation of cell migration by extracellular matrix mechanics at a glance.Journal of cell science · 2025Review
- EMT-related cell-matrix interactions are linked to states of cell unjamming in cancer spheroid invasion.iScience · 2024Article
- A Multicellular Mechanochemical Model to Investigate Tumor Microenvironment Remodeling and Pre-Metastatic Niche Formation.Cellular and molecular bioengineering · 2024Article
- Intercellular junction-driven stromal cell stacking in a confined 3D microcavity.APL bioengineering · 2024Article
- Recent advances in shape memory scaffolds and regenerative outcomes.Biomedical engineering letters · 2024Review
- Confinement primes cells for faster migration by polarizing active mitochondria.Nanoscale advances · 2023Article
- Research of restricted migration evaluation of MDA-MB-231 cells in 2D and 3D co-culture models.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Cell jamming in a collagen-based interface assay is tuned by collagen density and proteolysis.Journal of cell science · 2023Article
- A dynamic biomimetic model of the membrane-bound CD4-CD3-TCR complex during pMHC disengagement.Biophysical journal · 2023Article
- [A cervical cancer tissue-derived decellularized extracellular matrix scaffold for cervical cancer tissue reconstructionNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- The emerging role of microtubules in invasion plasticity.Frontiers in oncology · 2023Review
- AGE-breaker ALT711 reverses glycation-mediated cancer cell migration.Soft matter · 2022Article
- Link between glucose metabolism and epithelial-to-mesenchymal transition drives triple-negative breast cancer migratory heterogeneity.iScience · 2022Article
- Cancer-Associated Fibroblasts in a 3D Engineered Tissue Model Induce Tumor-like Matrix Stiffening and EMT Transition.Cancers · 2022Article
1 more citing papers are in PubMed but not listed here.
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8 authors at 1 institution in 1 country.
Funding
Abstract
Tumor cell invasion through the stromal extracellular matrix (ECM) is a key feature of cancer metastasis, and understanding the cellular mechanisms of invasive migration is critical to the development of effective diagnostic and therapeutic strategies. Since cancer cell migration is highly adaptable to physiochemical properties of the ECM, it is critical to define these migration mechanisms in a context-specific manner. Although extensive work has characterized cancer cell migration in two- and three-dimensional (3D) matrix environments, the migration program employed by cells to move through native and cell-derived microtracks within the stromal ECM remains unclear. We previously reported the development of an in vitro model of patterned type I collagen microtracks that enable matrix metalloproteinase-independent microtrack migration. Here we show that collagen microtracks closely resemble channel-like gaps in native mammary stroma ECM and examine the extracellular and intracellular mechanisms underlying microtrack migration. Cell-matrix mechanocoupling, while critical for migration through 3D matrix, is not necessary for microtrack migration. Instead, cytoskeletal dynamics, including actin polymerization, cortical tension, and microtubule turnover, enable persistent, polarized migration through physiological microtracks. These results indicate that tumor cells employ context-specific mechanisms to migrate and suggest that selective targeting of cytoskeletal dynamics, but not adhesion, proteolysis, or cell traction forces, may effectively inhibit cancer cell migration through preformed matrix microtracks within the tumor stroma.
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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.