Biophysical Society Thematic Meeting | Riga 2026

Active and Responsive Soft Matter: From Biological to Engineered Systems

Thursday Speaker Abstracts

MATRIX STRESS RELAXATION PROMOTES GLIOBLASTOMA CELL MIGRATION IN A LIGAND-SPECIFIC MANNER Katarzyna Pogoda 1 ; Konrad Zochowski 2 ; Monika Szczepanek-Dulska 1 ; Magdalena Zakrzewska 2 ; Mariusz Sawieljew 2 ; Ewelina Piktel 2 ; Robert Bucki 2 ; 1 Institute of Nuclear Physics PAN, Department of Biological Physics and Nanospectroscopy, Krakow, Poland 2 Medical University of Bialystok, Department of Medical Microbiology and Nanobiomedical Engineering, Bialystok, Poland Glioblastoma multiforme (GBM) invasion is strongly influenced by the mechanical and biochemical properties of the extracellular matrix (ECM). While substrate stiffness has been extensively studied, the role of matrix viscosity in regulating GBM migration remains insufficiently understood. Here, we investigated how substrate viscoelasticity and adhesion ligand identity modulate the migration behavior and mechanotransduction-related gene expression of LN-229 glioblastoma cells. Polyacrylamide hydrogels with comparable storage modulus (G′ ≈ 1 kPa) but increasing loss modulus (G″ ≈ 5 –250 Pa) were prepared to selectively vary substrate viscosity. Hydrogels were functionalized with type I collagen, fibronectin, or laminin. Cell migration was analyzed using time-lapse microscopy and single-cell trajectory reconstruction, while morphology was evaluated by fluorescence imaging. Additionally, expression of migration- and adhesion-related genes was assessed using quantitative RT-PCR. The effect of substrate viscoelasticity on glioblastoma migration strongly depended on the adhesion ligand. On collagen- coated substrates, increasing G″ enhanced migration speed by ~25% and net displacement by ~150%, accompanied by a shift toward more persistent random walk-type migration. In contrast, fibronectin-coated substrates showed limited sensitivity to viscosity changes. Laminin-coated substrates induced lower migration speed and persistence despite broad activation of mechanotransduction- and invasion-related genes, including PTK2B, SRC, MMP14, and IGF1R. Cell morphology was determined mainly by adhesion ligand identity rather than substrate viscosity. These findings demonstrate that matrix stress relaxation is not a universal promoter of glioblastoma invasion but rather acts as a context-dependent regulator shaped by specific adhesion signaling pathways. The results highlight the importance of integrating both mechanical and biochemical ECM properties in the development of anti invasive therapeutic strategies for GBM.

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