Journal
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
Volume 10, Issue 3, Pages -Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a029330
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Funding
- Netherlands Organization for Scientific Research [NWO/ZonMW-VIDI 016.096.318]
- Foundation Vrienden UMC Utrecht [11.081]
- Dutch Cancer Society [KWF-UU-2011-5230, KWF-UU-2014-7201, KWF-UU-2016-10456]
- Derksen laboratory
- van Diest laboratory
- [H2020-FETPROACT/2016-2017/731957]
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Classical cadherins are the key molecules that control cell-cell adhesion. Notwithstanding this function, it is also clear that classical cadherins are more than just the glue that keeps the cells together. Cadherins are essential regulators of tissue homeostasis that govern multiple facets of cellular function and development, by transducing adhesive signals to a complex network of signaling effectors and transcriptional programs. In cancer, cadherins are often inactivated or functionally inhibited, resulting in disease development and/or progression. This review focuses on E-cadherin and its causal role in the development and progression of breast and gastric cancer. We provide a summary of the biochemical consequences and consider the conceptual impact of early (mutational) E-cadherin loss in cancer. We advocate that carcinomas driven by E-cadherin loss should be considered actin-diseases, caused by the specific disruption of the E-cadherin-actin connection and a subsequent dependence on sustained actomyosin contraction for tumor progression. Based on the available data from mouse and human studies we discuss opportunities for targeted clinical intervention.
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