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

K. M. Brannon, C. M. Million Passe, C. R. White, N. A. Bade, M. W. King, C. C. Quirk

Research output: Contribution to journalArticle

14 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)146-155
Number of pages10
JournalCancer Letters
Volume254
Issue number1
DOIs
StatePublished - Aug 28 2007

Keywords

  • Aneuploidy
  • Cell cycle
  • HMG
  • p21
  • p27
  • p57
  • p8
  • Senescence
  • Tumorigenesis

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology
  • Oncology

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