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Kanemura, Y.

Publications and source records attributed to Kanemura, Y..

2 recordsLinked to original sources

Mechanical polarity links adhesion-tuned protrusions to directional stability in glioblastoma cell migration

Glioblastoma invasion critically limits therapeutic outcomes, and understanding the physical principles that govern cell motility is essential for developing effective therapies. Here, to clarify the mechanical links between cell adhesion, protrusions, and migration, we analyzed glioblastoma-derived cells migrating on fibronectin- and laminin-coated extracellular matrix (ECM) substrates using time-lapse imaging and mathematical modeling. We quantified cell motility on each ECM and constructed a coarse-grained biophysical model that incorporates catch- and slip-bond kinetics. We treated the ECM as an external boundary condition that modulates adhesion dynamics, distinct from the intrinsic mechanical parameters of the cell. The model reproduced ECM-dependent differences in cell motility. The results suggest that adhesions and protrusion elongation on fibronectin are less stable than on laminin, and opposing forces between protrusions reduce net displacement more strongly on fibronectin than on laminin, leading to less coordinated tensile forces. Based on these results, we establish mechanical polarity, defined as an imbalance of protrusion- and adhesion-mediated forces that drive directional migration, as a quantifiable physical principle of cell protrusion and migration. This principle likely extends beyond glioblastoma biology, providing a generalizable mechanism that links adhesion dynamics to migration stability and offering a physical basis for strategies to suppress invasive cell behavior.

systems biology↗

Weak and tunable adhesion-clutch drives rapid cell migration and glioblastoma motility

To move forward, migrating cells must exert backward forces against the extracellular environment. Recent studies have highlighted the importance of integrin-independent forces for cell migration; but the molecular machinery that exerts forces remains unclear. Here, we show that the clutch-linker molecule shootin1 and the cell adhesion molecule L1 transmit the backward force of treadmilling actin filaments to the adhesive environment for rapid dendritic cell migration. Notably, shootin1 and L1 transmit weak traction forces, [~]100 times weaker than integrin-based forces, by constituting an integrin-independent slippery adhesion-clutch. This adhesion-clutch system is tunable in response to the chemoattractant CCL19 and the adhesive ligand laminin and mediates chemotaxis through its polarized activation within cells. Furthermore, its aberrant activity enhances glioblastoma cell motility. Our results show that the weak adhesion-clutch is well-suited for rapid cell migration, without forming strong adhesions that impede cell motility, and provides a potential target for inhibiting abnormal cell motility.

cell biology↗