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• W2023608795 abstract "Solid tumors are characterized by high interstitial fluid pressure, which drives fluid efflux from the tumor core. Tumor-associated interstitial flow (IF) at a rate of ∼3 µm/s has been shown to induce cell migration in the upstream direction (rheotaxis). However, the molecular biophysical mechanism that underlies upstream cell polarization and rheotaxis remains unclear. We developed a microfluidic platform to investigate the effects of IF fluid stresses imparted on cells embedded within a collagen type I hydrogel, and we demonstrate that IF stresses result in a transcellular gradient in β1-integrin activation with vinculin, focal adhesion kinase (FAK), FAK(PY397), F actin, and paxillin-dependent protrusion formation localizing to the upstream side of the cell, where matrix adhesions are under maximum tension. This previously unknown mechanism is the result of a force balance between fluid drag on the cell and matrix adhesion tension and is therefore a fundamental, but previously unknown, stimulus for directing cell movement within porous extracellular matrix." @default.
• W2023608795 created "2016-06-24" @default.
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• W2023608795 date "2014-02-03" @default.
• W2023608795 modified "2023-10-11" @default.
• W2023608795 title "Mechanotransduction of fluid stresses governs 3D cell migration" @default.
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• W2023608795 doi "https://doi.org/10.1073/pnas.1316848111" @default.
• W2023608795 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3932905" @default.
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• W2023608795 hasPublicationYear "2014" @default.
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