Type I collagen down-regulates E-cadherin expression by increasing PI3KCA in cancer cells

被引：56

作者：

Cheng, Jung-Chien ^{[1
]}

Leung, Peter C. K. ^{[1
]}

机构：

[1] Univ British Columbia, Dept Obstet & Gynecol, Child & Family Res Inst, Vancouver, BC V6H 3V5, Canada

来源：

CANCER LETTERS | 2011年 / 304卷 / 02期

基金：

加拿大健康研究院;

关键词：

E-cadherin; Collagen I; Extracellular matrix; Epithelial-mesenchymal transition; EPITHELIAL-MESENCHYMAL TRANSITION; INTEGRIN-LINKED KINASE; TUMOR PROGRESSION; CARCINOMA-CELLS; PANCREATIC-CARCINOMA; UP-REGULATION; ADHESION; MIGRATION; PROMOTES; MICROENVIRONMENT;

D O I：

10.1016/j.canlet.2011.02.008

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

The extracellular matrix (ECM) has been shown to induce the epithelial-mesenchymal transition (EMT), which is characterized by the loss of E-cadherin. However, little is known about the mechanisms by which collagen I, the most abundant component of ECM, induces this process. Here, we show that E-cadherin was down-regulated in response to collagen I in SKOV3 ovarian cancer cells and PC3 prostate cancer cells. Furthermore, collagen I induced the up-regulation of PIK3CA. which in turn contributed to the collagen I-induced down-regulation of E-cadherin by up-regulating its transcriptional repressors, Snail and Slug. Our data demonstrate that PIK3CA is a mediator of collagen I-induced down-regulation of E-cadherin. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

引用

页码：107 / 116

页数：10

共 35 条

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Cell adhesion and signalling by cadherins and Ig-CAMs in cancer [J].