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

Abstract
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.
AuthorsSelwin K Wu, Anne K Lagendijk, Benjamin M Hogan, Guillermo A Gomez, Alpha S Yap
JournalCell cycle (Georgetown, Tex.) (Cell Cycle) Vol. 14 Issue 3 Pg. 315-22 ( 2015) ISSN: 1551-4005 [Electronic] United States
PMID25590779 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Actins
  • Cadherins
  • Wiskott-Aldrich Syndrome Protein, Neuronal
  • Myosin Type II
  • HRAS protein, human
  • Proto-Oncogene Proteins p21(ras)
Topics
  • Actins (metabolism)
  • Animals
  • Caco-2 Cells
  • Cadherins (metabolism)
  • Epithelium (metabolism)
  • Humans
  • Intercellular Junctions (metabolism)
  • Models, Biological
  • Myosin Type II (metabolism)
  • Neoplasms (metabolism, pathology)
  • Proto-Oncogene Proteins p21(ras)
  • Wiskott-Aldrich Syndrome Protein, Neuronal (metabolism)

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