4.7 Article

Expression of the high mobility group A family member p8 is essential to maintaining tumorigenic potential by promoting cell cycle dysregulation in LβT2 cells

期刊

CANCER LETTERS
卷 254, 期 1, 页码 146-155

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2007.03.011

关键词

p8; HMG; cell cycle; senescence; aneuploidy; tumorigenesis; p21; p27; p57

类别

向作者/读者索取更多资源

The mechanism by which the HMGA protein p8 facilitates tumorigenesis may be cell cycle dysregulation. Control- (C) L beta T2 cells, which express p8, form tumors at a rate five-times faster than p8-knockdown (p8-KD)-L beta T2 cells. In association with this heightened tumorigenic potential, p8-expressing C-L beta T2 cells avoid G(0)/G(1) arrest and become genetically unstable while p8-KD-L beta T2 cells arrest in G(0)/G(1), become senescent upon overgrowth, and maintain a diploid population. These phenotypic changes correspond to altered cell cycle regulation at the G(1)-to-S transition that may be due to p8-mediated changes in expression of the Cip/Kip family members of cell cycle inhibitors, p21, p27, and p57. (c) 2007 Elsevier Ireland Ltd. All rights reserved.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据