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
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.
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