E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer

被引：671

作者：

Schmalhofer, Otto ^{[1
]}

Brabletz, Simone ^{[1
]}

Brabletz, Thomas ^{[1
]}

机构：

[1] Univ Freiburg, Dept Visceral Surg, D-79106 Freiburg, Germany

来源：

CANCER AND METASTASIS REVIEWS | 2009年 / 28卷 / 1-2期

关键词：

E-cadherin; EMT; ZEB1; Cancer; Invasion; Feedback/forward loop; EPITHELIAL-MESENCHYMAL TRANSITION; TRANSCRIPTION FACTOR ZEB1; ZINC-FINGER PROTEIN; HAIR FOLLICLE MORPHOGENESIS; CELL-ADHESION MOLECULE; WNT SIGNALING PATHWAY; REPRESSES E-CADHERIN; REGULATES E-CADHERIN; GROWTH-FACTOR-I; COLORECTAL-CANCER;

D O I：

10.1007/s10555-008-9179-y

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The embryonic program 'epithelial-mesenchymal transition' (EMT) is activated during tumor invasion in disseminating cancer cells. Characteristic to these cells is a loss of E-cadherin expression, which can be mediated by EMT-inducing transcriptional repressors, e.g. ZEB1. Consequences of a loss of E-cadherin are an impairment of cell-cell adhesion, which allows detachment of cells, and nuclear localization of beta-catenin. In addition to an accumulation of cancer stem cells, nuclear beta-catenin induces a gene expression pattern favoring tumor invasion, and mounting evidence indicates multiple reciprocal interactions of E-cadherin and beta-catenin with EMT-inducing transcriptional repressors to stabilize an invasive mesenchymal phenotype of epithelial tumor cells.

引用

页码：151 / 166

页数：16

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