CCN6 (WISP3) as a new regulator of the epithelial phenotype in breast cancer
CCN6 (WISP3) as a new regulator of the epithelial phenotype in breast cancer
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DOI：
10.1159/000101308
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发表时间：
2007-01-01
影响因子：
2.7
通讯作者：
Merajver, Sofia D.
中科院分区：
文献类型：
--
作者：
Kleer, Celina G.;Zhang, Yanhong;Merajver, Sofia D.
CCN 6（WISP 3）是属于CCN（Cyr 61，CTGF，Nov）基因家族的富含半胱氨酸的分泌蛋白。我们发现，在80%的局部晚期乳腺癌（炎性乳腺癌）中，CCN 6 mRNA减少。CCN 6包含四个高度保守的基序，与胰岛素样生长因子结合蛋白、血管性血友病C型、血小板反应蛋白1和参与二聚化的羧基末端结构域pupirin具有序列相似性。CCN 6在乳腺癌中具有肿瘤生长、增殖和侵袭抑制功能。最近，通过使用小干扰RNA下调永生化人乳腺上皮细胞中的CCN 6，发现CCN 6是诱导上皮-间质转化（EMT）过程所必需的，其抑制E-cadherin基因表达并诱导EMT特征性蛋白表达程序。本综述将重点介绍CCN 6在乳腺癌中的功能，特别强调CCN 6作为乳腺上皮表型和E-钙粘蛋白表达的调节剂的新作用。版权所有（c）2007 S. Karger AG，巴塞尔。
CCN6 (WISP3) is a cysteine-rich secreted protein that belongs to the CCN (Cyr61, CTGF, Nov) family of genes. We found that CCN6 mRNA is reduced in 80% of cases of the most lethal form of locally advanced breast cancer, inflammatory breast cancer. CCN6 contains four highly conserved motifs with sequence similarities to insulin-like growth factor binding proteins, von Willebrand type C, thrombospondin 1, and a carboxyl-terminal domain putatively involved in dimerization. CCN6 has tumor growth-, proliferation-, and invasion-inhibitory functions in breast cancer. Recently, by using a small infering RNA to downregulate CCN6 in immortalized human mammary epithelial cells, CCN6 was found to be essential to induce the process of epithelial-mesenchymal transition (EMT) with repression of E-cadherin gene expression and induction of a protein expression program characteristic of EMT. This review will focus on the current knowledge regarding the function of CCN6 in breast cancer with special emphasis on the emerging role of CCN6 as a regulator of the epithelial phenotype and E-cadherin expression in the breast. Copyright (c) 2007 S. Karger AG, Basel.