ArticleBiophysical journal2019
Are the Effects of Independent Biophysical Factors Linearly Additive? A 3D Tumor Migration Model.
Article in Biophysical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- Proteolysis at the extracellular matrix interface: Molecular architects and regulators in health and disease.The FEBS journal · 2026Review
- Cancer cell response to extrinsic and intrinsic mechanical cue: opportunities for tumor apoptosis strategies.Regenerative biomaterials · 2024Review
- Fluid flow to mimic organ function in 3DAPL bioengineering · 2023Review
- Unravelling cell migration: defining movement from the cell surface.Cell adhesion & migration · 2022Review
- Computational estimates of mechanical constraints on cell migration through the extracellular matrix.PLoS computational biology · 2020Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Interstitial fluid flow plays a critical role in tumor cell invasion, yet this role has not been explored extensively in combination with other microenvironmental factors. Here, we establish a novel computational model of three-dimensional breast cancer cell migration to unveil the effect of interstitial fluid flow in the dependence of various extracellular matrix (ECM) physical properties. Our model integrates several principal factors: fluid dynamics, autologous chemotaxis, collagen fiber network structure, ECM stiffness, and cell-fiber and cell-flow interaction. First, independently with an aligned collagen fiber network and interstitial fluid flow, this model is validated by successfully reproducing the cell migration patterns. In the model, the interstitial fluid flow leads to directional symmetry breaking of chemotactic migration and synergizes with the ECM orientation to regulate cell migration. This synergy is universal in both the mesenchymal and the amoeboid migration modes, despite the fact that the cell-ECM interaction are different. Consequently, we construct a cell displacement function depending on these factors. Our cell migration model enables three-dimensional cancer migration prediction, mechanism exploration, and inhibition treatment design in a complex tumor microenvironment.
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Registered trials
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