Active contractility at E-cadherin junctions and its implications for cell extrusion in cancer

Cell Cycle. 2015;14(3):315-22. doi: 10.4161/15384101.2014.989127.


Cellular contractility regulates tissue cohesion and morphogenesis. In epithelia, E-cadherin adhesion couples the contractile cortices of neighboring cells together to produce tension at junctions that can be transmitted across the epithelium in a planar fashion. We have recently demonstrated that contractility is also patterned in the apical-lateral axis within epithelial junctions. Our findings highlight the role that cytoskeletal regulation plays in controlling the levels of intra-junctional tension. Of note, dysregulation of this apicolateral pattern of tension can drive oncogenic cell extrusion. In this article, we provide a detailed description of the actomyosin cytoskeleton organization during oncogenic extrusion and discuss the implications of cell extrusion in cancer.

Keywords: E-Cadherin; actin; cell extrusion; myosin; oncogene.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Caco-2 Cells
  • Cadherins / metabolism*
  • Epithelium / metabolism
  • Humans
  • Intercellular Junctions / metabolism*
  • Models, Biological
  • Myosin Type II / metabolism
  • Neoplasms / metabolism*
  • Neoplasms / pathology*
  • Proto-Oncogene Proteins p21(ras)
  • Wiskott-Aldrich Syndrome Protein, Neuronal / metabolism


  • Actins
  • Cadherins
  • Wiskott-Aldrich Syndrome Protein, Neuronal
  • Myosin Type II
  • HRAS protein, human
  • Proto-Oncogene Proteins p21(ras)