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@ARTICLE{GaikoShcherbak:891636,
      author       = {Gaiko-Shcherbak, Aljona and Eschenbruch, Julian and
                      Kronenberg, Nils M. and Teske, Michael and Wolters, Benjamin
                      and Springer, Ronald and Gather, Malte C. and Merkel, Rudolf
                      and Hoffmann, Bernd and Noetzel, Erik},
      title        = {{C}ell {F}orce-{D}riven {B}asement {M}embrane {D}isruption
                      {F}uels {EGF}- and {S}tiffness-{I}nduced {I}nvasive {C}ell
                      {D}issemination from {B}enign {B}reast {G}land {A}cini},
      journal      = {International journal of molecular sciences},
      volume       = {22},
      number       = {8},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {FZJ-2021-01632},
      pages        = {3962 -},
      year         = {2021},
      abstract     = {Local basement membrane (BM) disruption marks the initial
                      step of breast cancer invasion. The activation mechanisms of
                      force-driven BM-weakening remain elusive. We studied the
                      mechanical response of MCF10A-derived human breast cell
                      acini with BMs of tuneable maturation to physical and
                      soluble tumour-like extracellular matrix (ECM) cues.
                      Traction force microscopy (TFM) and elastic resonator
                      interference stress microscopy (ERISM) were used to quantify
                      pro-invasive BM stress and protrusive forces. Substrate
                      stiffening and mechanically impaired BM scaffolds induced
                      the invasive transition of benign acini synergistically.
                      Robust BM scaffolds attenuated this invasive response.
                      Additional oncogenic EGFR activation compromised the BMs’
                      barrier function, fuelling invasion speed and incidence.
                      Mechanistically, EGFR-PI3-Kinase downstream signalling
                      modulated both MMP- and force-driven BM-weakening processes.
                      We show that breast acini form non-proteolytic and
                      BM-piercing filopodia for continuous matrix
                      mechanosensation, which significantly push and pull on the
                      BM and ECM under pro-invasive conditions. Invasion-triggered
                      acini further shear and compress their BM by
                      contractility-based stresses that were significantly
                      increased (3.7-fold) compared to non-invasive conditions.
                      Overall, the highest amplitudes of protrusive and
                      contractile forces accompanied the highest invasiveness.
                      This work provides a mechanistic concept for tumour
                      ECM-induced mechanically misbalanced breast glands fuelling
                      force-driven BM disruption. Finally, this could facilitate
                      early cell dissemination from pre-invasive lesions to
                      metastasize eventually.},
      cin          = {IBI-2},
      ddc          = {540},
      cid          = {I:(DE-Juel1)IBI-2-20200312},
      pnm          = {524 - Molecular and Cellular Information Processing
                      (POF4-524) / DFG project 273723265 - Mechanosensation und
                      Mechanoreaktion in epidermalen Systemen},
      pid          = {G:(DE-HGF)POF4-524 / G:(GEPRIS)273723265},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {33921304},
      UT           = {WOS:000644316700001},
      doi          = {10.3390/ijms22083962},
      url          = {https://juser.fz-juelich.de/record/891636},
}