Molecular mechanisms controlling E-cadherin expression in breast cancer

被引：267

作者：

Baranwal, Somesh

Alahari, Suresh K. ^{[1
,2
]}

机构：

[1] Louisiana State Univ, Dept Biochem & Mol Biol, Stanley S Scott Canc Ctr, Hlth Sci Ctr, New Orleans, LA 70112 USA

[2] Louisiana State Univ, Hlth Sci Ctr, Stanley Scott Canc Ctr, New Orleans, LA 70112 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 384卷 / 01期

关键词：

E-Cadherin; Breast cancer; Zinc-finger transcription factor; miRNA; EPITHELIAL-MESENCHYMAL TRANSITION; TUMOR-METASTASIS; N-CADHERIN; TRANSCRIPTIONAL REPRESSOR; PROMOTES METASTASIS; MASTER REGULATOR; CELL-ADHESION; SNAIL; PROGRESSION; INVASION;

D O I：

10.1016/j.bbrc.2009.04.051

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

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 Ca2+-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. (c) 2009 Elsevier Inc. All rights reserved.

引用

页码：6 / 11

页数：6

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