p53 arrests growth and induces differentiation of v-Myb-transformed monoblasts

Differentiation. 2007 Sep;75(7):592-604. doi: 10.1111/j.1432-0436.2006.00158.x. Epub 2007 Feb 16.

Abstract

The p53 protein can control cell cycle progression, programmed cell death, and differentiation of many cell types. Ectopic expression of p53 can resume capability of cell cycle arrest, differentiation, and apoptosis in various leukemic cell lines. In this work, we expressed human p53 protein in v-Myb-transformed chicken monoblasts. We found that even this protein possessing only 53% amino acid homology to its avian counterpart can significantly alter morphology and physiology of these cells causing the G2-phase cell cycle arrest and early monocytic differentiation. Our results document that the species-specific differences of the p53 molecules, promoters/enhancers, and co-factors in avian and human cells do not interfere with differentiation- and cell cycle arrest promoting capabilites of the p53 tumor suppressor even in the presence of functional v-Myb oncoprotein. The p53-induced differentiation and cell cycle arrest of v-Myb-transformed monoblasts are not associated with apoptosis suggesting that the p53-driven pathways controlling apoptosis and differentiation/proliferation are independent.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Cell Cycle / genetics
  • Cell Differentiation / genetics
  • Cell Differentiation / physiology*
  • Cell Line, Transformed
  • Cell Proliferation*
  • Chickens
  • G2 Phase / genetics
  • Growth Inhibitors / genetics
  • Growth Inhibitors / physiology*
  • Humans
  • Monocytes / cytology*
  • Oncogene Proteins v-myb / genetics*
  • Signal Transduction / genetics
  • Transfection
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / physiology*

Substances

  • Growth Inhibitors
  • Oncogene Proteins v-myb
  • Tumor Suppressor Protein p53