Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2116799 | Cancer Letters | 2007 | 10 Pages |
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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Authors
K.M. Brannon, C.M. Million Passe, C.R. White, N.A. Bade, M.W. King, C.C. Quirk,