Kindlin-2 promotes genome instability in breast cancer cells

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• 作者：Ting Zhao^a ; ^b ; ^c ; ¹ ; Lizhao Guan^a ; ^b ; ¹ ; Yu Yu^a ; ^b ; Xuelian Pei^a ; ^b ; Jun Zhan^a ; ^b ; Ling Han^d ; Yan Tang^a ; ^b ; Feng Li^a ; ^b ; Weigang Fang^a ; ^c ; ^{wgfang@bjmu.edu.cn} ; Hongquan Zhang^a ; ^b ; ^{Hongquan.Zhang@bjmu.edu.cn}
• 关键词：Kindlin-2 ; Breast cancer ; Genome instability ; Tumor formation
• 刊名：Cancer Letters
• 出版年：2013
• 出版时间：28 April, 2013
• 年：2013
• 卷：330
• 期：2
• 页码：208-216
• 全文大小：1463 K

文摘

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.