Kindlin-2 promotes genome instability in breast cancer cells
Kindlin-2 promotes genome instability in breast cancer cells
复制标题
Kindlin-2 促进乳腺癌细胞基因组不稳定
DOI：
10.1016/j.canlet.2012.11.043
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发表时间：
2013-04-28
期刊：
影响因子：
9.7
通讯作者：
Zhang, Hongquan
中科院分区：
文献类型：
--
作者：
Zhao, Ting;Guan, Lizhao;Zhang, Hongquan
Kindlin-2作为一种粘着斑蛋白，已被发现调节肿瘤的进展。然而，Kindlin-2调节肿瘤进展的潜在机制在很大程度上是未知的。在这里，我们报告说，Kindlin-2调节乳腺癌细胞增殖，凋亡和染色体异常的功能测定的获得和丧失。在功能上，Kindlin-2的过表达促进移植的异种移植物中的肿瘤形成，而Kindlin-2的敲低抑制小鼠中的肿瘤生长。从机制上讲，基于阵列的比较基因组杂交和核型分析表明，Kindlin-2的异位表达导致乳腺癌细胞中基因组的不稳定性。我们的数据表明Kindlin-2通过诱导基因组不稳定性调节乳腺癌进展的新机制。(C)2012爱思唯尔爱尔兰有限公司保留所有权利。
Kindlin-2, as a focal adhesion protein, has been found to regulate tumor progression. However, the mechanism underlying Kindlin-2 regulation of tumor progression is largely unknown. Here, we report that Kindlin-2 regulates breast cancer cell proliferation, apoptosis and chromosomal abnormalities in both gain and loss of function assays. Functionally, overexpression of Kindlin-2 promotes tumor formation in implanted xenograft while knockdown of Kindlin-2 inhibits tumor growth in mice. Mechanistically, an array-based comparative genomic hybridization and karyotype analyses indicate that ectopic expression of Kindlin-2 leads to genome instability in breast cancer cells. Our data suggest a novel mechanism that Kindlin-2 regulates breast cancer progression by inducing genome instability. (C) 2012 Elsevier Ireland Ltd. All rights reserved.