کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2113091 | 1546692 | 2013 | 9 صفحه PDF | دانلود رایگان |

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.
► Kindlin-2 promotes tumor growth in breast cancer cells.
► Kindlin-2 prevents apoptosis in breast cancer cells.
► Ectopic expression of Kindlin-2 leads to genome instability in breast cancer cells.
Journal: Cancer Letters - Volume 330, Issue 2, 28 April 2013, Pages 208–216