ArticleMaterials today. Bio2025
Myosin-actin pattern links matrix stiffness to GFAT2-hyaluronan metabolism.
Article in Materials today. Bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Piezo1-mediated mechanotransduction and metabolic regulation in bone health: molecular mechanisms and implications for bone disorders.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
7 authors.
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Abstract
While dysregulated extracellular matrix deposition and stiffening are known to drive tumor progression, breast cancer cells can persist, relapse, and metastasize to soft microenvironments. The distinct strategies that tumor cells adapted to soft matrices remain to be further explored. Here, we report that breast tumor cells exploit soft matrices to activate GFAT2-mediated hyaluronan metabolism that can modulate macrophages. This process is driven by the upregulation of GFAT2 expression through enhanced nuclear translocation of NF-κB and XBP1s, coupled with elevated GFAT activity and subsequent hyaluronan production via suppressed AMPKα phosphorylation. Mechanistically, the expression and activity of GFAT2 are jointly modulated by the total cellular levels of myosin and F-actin. More specifically, the ROCK-Rac1 balance, which can regulate both the cortical-to-cytoplasmic ratio of active myosin and the circumferential arrangement of cortical F-actin, mediates the NF-κB-XBP1s-GFAT2 signaling axis. Furthermore, our
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