Abstract
Disruption of cell–cell adhesion, which is essential for the maintenance of epithelial plasticity and is mediated by a class of proteins called cadherins, is an initial event in the progression of cancer. Cadherins are Ca 2+-dependent transmembrane proteins that are associated with actin via other cytoplasmic proteins. Disruption of cell–cell adhesion during cancer progression is an important event during cancer initiation and metastasis. E-cadherin, one of the most widely studied tumor suppressors in breast cancer, belongs to a family of calcium-dependent cell adhesion molecules. Various signaling molecules and transcription factors regulate the expression of E-cadherin. Loss of E-cadherin has been reported to induce epithelial–mesenchymal transition in several cancers. This review highlights recent advances in defining the mechanisms that regulate E-cadherin expression in breast cancer.
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