4.6 Article

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

期刊

CELL CYCLE
卷 14, 期 3, 页码 315-322

出版社

TAYLOR & FRANCIS INC
DOI: 10.4161/15384101.2014.989127

关键词

actin; cell extrusion; E-Cadherin; myosin; oncogene

资金

  1. National Health and Medical Research Council of Australia [631383, 1010489, 1037320, 1044041, 1067405]
  2. Australian Research Council [DP120104667]
  3. National Breast Cancer Foundation (Australia) [CG-10-04]
  4. Kids Cancer Project of The Oncology Children's Foundation
  5. University of Queensland Early Career Grant [2012003354]
  6. University of Queensland Postdoctoral Fellowship
  7. National Breast Cancer Foundation [CG-10-04] Funding Source: researchfish

向作者/读者索取更多资源

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.

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