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.

• Authors: Selwin K Wu, Anne K Lagendijk, Benjamin M Hogan, Guillermo A Gomez, Alpha S Yap
• Journal: Cell cycle (Georgetown, Tex.) (Cell Cycle) Vol. 14 Issue 3 Pg. 315-22 ( 2015) ISSN: 1551-4005 [Electronic] United States
• PMID: 25590779 (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)