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Cold Spring Harb Perspect Biol. 2018 Mar 1;10(3). pii: a029330. doi: 10.1101/cshperspect.a029330.

Loss of E-Cadherin-Dependent Cell-Cell Adhesion and the Development and Progression of Cancer.

Author information

1
Department of Medicine, University of California at San Diego, La Jolla, California 92093.
2
Department of Pathology, University Medical Center Utrecht, Utrecht 3584CX, The Netherlands.

Abstract

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.

PMID:
28507022
DOI:
10.1101/cshperspect.a029330
[Indexed for MEDLINE]

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