Article ID Journal Published Year Pages File Type
2116799 Cancer Letters 2007 10 Pages PDF
Abstract
The mechanism by which the HMGA protein p8 facilitates tumorigenesis may be cell cycle dysregulation. Control- (C) LβT2 cells, which express p8, form tumors at a rate five-times faster than p8-knockdown (p8-KD)-LβT2 cells. In association with this heightened tumorigenic potential, p8-expressing C-LβT2 cells avoid G0/G1 arrest and become genetically unstable while p8-KD-LβT2 cells arrest in G0/G1, become senescent upon overgrowth, and maintain a diploid population. These phenotypic changes correspond to altered cell cycle regulation at the G1-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.
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Life Sciences Biochemistry, Genetics and Molecular Biology Cancer Research
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