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

被引:23
作者
Brannon, K. M.
Passe, C. M. Million
White, C. R.
Bade, N. A.
King, M. W.
Quirk, C. C.
机构
[1] Indiana Univ, Sch Med, Dept Biol, Med Sci Program Indiana, Bloomington, IN 47405 USA
[2] Indiana Univ, Sch Med, Med Sci Program, Bloomington, IN USA
[3] Indiana Univ, Sch Med, Interdisciplinary Grad Program Biochem, Bloomington, IN USA
[4] Indiana Univ, Sch Med, Dept Biochem & Mol Biol, Terre Haute, IN USA
关键词
p8; HMG; cell cycle; senescence; aneuploidy; tumorigenesis; p21; p27; p57;
D O I
10.1016/j.canlet.2007.03.011
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:146 / 155
页数:10
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