Dresden 2020 – scientific programme
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BP: Fachverband Biologische Physik
BP 30: Cell Adhesion and Migration, Multicellular Systemadhesion and Migration, Multicellular Systems II
BP 30.7: Talk
Thursday, March 19, 2020, 11:45–12:00, HÜL 386
Cell-cell adhesion and 3D matrix confinement explain plasticity of breast cancer invasion — •Simon Syga1, Peter Friedl2, and Andreas Deutsch1 — 1Center for Information Services and High Performance Computing, Technische Universität Dresden, Dresden, Germany — 2Department of Cell Biology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands
Plasticity of cancer invasion and metastasis depends on the ability of cancer cells to switch between collective invasion modes and single cell dissemination, under the control of cadherin-mediated cell-cell junctions. E-cadherin is considered a tumor suppressor, the downregulation of which causes single-cell scattering in 2D environments. In clinical samples, however, E-cadherin expressing and deficient tumors both invade collectively and metastasize equally, implicating additional mechanisms controlling cell-cell cooperation and dissemination.
Using a cellular automaton model we identify physical confinement by the extracellular matrix (ECM) as the dominant physical mechanism that supports collective invasion irrespective of the composition and stability of cell-cell junctions. In particular, we predict that downregulation of E-cadherin results in a transition from coordinated to uncoordinated collective movement along extracellular boundaries, whereas single-cell escape depends on locally free tissue space.