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@ARTICLE{Eschenbruch:894790,
      author       = {Eschenbruch, Julian and Dreissen, Georg and Springer,
                      Ronald and Konrad, Jens and Merkel, Rudolf and Hoffmann,
                      Bernd and Noetzel, Erik},
      title        = {{F}rom {M}icrospikes to {S}tress {F}ibers: {A}ctin
                      {R}emodeling in {B}reast {A}cini {D}rives {M}yosin
                      {II}-{M}ediated {B}asement {M}embrane {I}nvasion},
      journal      = {Cells},
      volume       = {10},
      number       = {8},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {FZJ-2021-03392},
      pages        = {1979 -},
      year         = {2021},
      abstract     = {The cellular mechanisms of basement membrane (BM) invasion
                      remain poorly understood. We investigated the
                      invasion-promoting mechanisms of actin cytoskeleton
                      reorganization in BM-covered MCF10A breast acini.
                      High-resolution confocal microscopy has characterized actin
                      cell protrusion formation and function in response to
                      tumor-resembling ECM stiffness and soluble EGF stimulation.
                      Traction force microscopy quantified the mechanical BM
                      stresses that invasion-triggered acini exerted on the
                      BM–ECM interface. We demonstrate that acini use
                      non-proteolytic actin microspikes as functional precursors
                      of elongated protrusions to initiate BM penetration and ECM
                      probing. Further, these microspikes mechanically widened the
                      collagen IV pores to anchor within the BM scaffold via
                      force-transmitting focal adhesions. Pre-invasive basal cells
                      located at the BM–ECM interface exhibited predominantly
                      cortical actin networks and actin microspikes. In response
                      to pro-invasive conditions, these microspikes accumulated
                      and converted subsequently into highly contractile stress
                      fibers. The phenotypical switch to stress fiber cells
                      matched spatiotemporally with emerging high BM stresses that
                      were driven by actomyosin II contractility. The activation
                      of proteolytic invadopodia with MT1-MMP occurred at later BM
                      invasion stages and only in cells already disseminating into
                      the ECM. Our study demonstrates that BM pore-widening
                      filopodia bridge mechanical ECM probing function and
                      contractility-driven BM weakening. Finally, these
                      EMT-related cytoskeletal adaptations are critical mechanisms
                      inducing the invasive transition of benign breast acini.},
      cin          = {IBI-2},
      ddc          = {570},
      cid          = {I:(DE-Juel1)IBI-2-20200312},
      pnm          = {5243 - Information Processing in Distributed Systems
                      (POF4-524) / DFG project 273723265 - Mechanosensation und
                      Mechanoreaktion in epidermalen Systemen},
      pid          = {G:(DE-HGF)POF4-5243 / G:(GEPRIS)273723265},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34440749},
      UT           = {WOS:000689047400001},
      doi          = {10.3390/cells10081979},
      url          = {https://juser.fz-juelich.de/record/894790},
}