Molecular mechanisms controlling E-cadherin expression in breast cancer.
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.
Baranwal
Somesh
S
Department of Biochemistry and Molecular Biology, LSU Health Science Center, New Orleans, LA 70112, USA.
Alahari
Suresh K
SK
D001943:Breast Neoplasms / Q000235:genetics* / Q000473:pathology*; D015820:Cadherins / Q000235:genetics*; D002448:Cell Adhesion / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D014158:Transcription, Genetic
D015820:Cadherins