1.
Cancer Lett
; 254(1): 146-55, 2007 Aug 28.
Artículo
en Inglés
| MEDLINE
| ID: mdl-17451874
RESUMEN
The mechanism by which the HMGA protein p8 facilitates tumorigenesis may be cell cycle dysregulation. Control- (C) LbetaT2 cells, which express p8, form tumors at a rate five-times faster than p8-knockdown (p8-KD)-LbetaT2 cells. In association with this heightened tumorigenic potential, p8-expressing C-LbetaT2 cells avoid G(0)/G(1) arrest and become genetically unstable while p8-KD-LbetaT2 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.