ArticleCell reports2023
Reciprocal intra- and extra-cellular polarity enables deep mechanosensing through layered matrices.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Microscale matrix defects suppress tension-dependent protrusions and stall collective cell migration.Cell reports · 2026Article
- Osteocytes under Mechanical Loading Regulate PC-3 Cancer Cell-Mineral Interactions during Early-Stage Metastasis to Bone.Advanced biology · 2025Article
- Emergent depth-mechanosensing of epithelial collectives regulates cell clustering and dispersal on layered matrices.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Fast yet force-effective mode of supracellular collective cell migration due to extracellular force transmission.PLoS computational biology · 2025Article
- A high throughput cell stretch device for investigating mechanobiologyAPL bioengineering · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Adherent cells migrate on layered tissue interfaces to drive morphogenesis, wound healing, and tumor invasion. Although stiffer surfaces are known to enhance cell migration, it remains unclear whether cells sense basal stiff environments buried under softer, fibrous matrix. Using layered collagen-polyacrylamide gel systems, we unveil a migration phenotype driven by cell-matrix polarity. Here, cancer (but not normal) cells with stiff base matrix generate stable protrusions, faster migration, and greater collagen deformation because of "depth mechanosensing" through the top collagen layer. Cancer cell protrusions with front-rear polarity produce polarized collagen stiffening and deformations. Disruption of either extracellular or intracellular polarity via collagen crosslinking, laser ablation, or Arp2/3 inhibition independently abrogates depth-mechanosensitive migration of cancer cells. Our experimental findings, validated by lattice-based energy minimization modeling, present a cell migration mechanism whereby polarized cellular protrusions and contractility are reciprocated by mechanical extracellular polarity, culminating in a cell-type-dependent ability to mechanosense through matrix layers.
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Registered trials
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