Growth arrest induced by wild-type p53 protein blocks cells prior to or near the restriction point in late G1 phase

Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9210-4. doi: 10.1073/pnas.89.19.9210.

Abstract

Conditional expression of wild-type (wt) p53 protein in a glioblastoma tumor cell line has been shown to be growth inhibitory. We have now more precisely localized the position in the cell cycle where growth arrest occurs. We show that growth arrest occurs prior to or near the restriction point in late G1 phase of the cell cycle. The effect of wt p53 protein on the expression of four immediate-early genes (c-FOS, c-JUN, JUN-B, and c-MYC), one delayed-early gene (ornithine decarboxylase), and two late-G1/S-phase genes (B-MYB and DNA polymerase alpha) was also examined. Of this subset of growth response genes, only the expression of B-MYB and DNA polymerase alpha was significantly repressed. The possibility that decreased expression of B-MYB may be an important component of growth arrest mediated by wt p53 protein is discussed.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Blotting, Northern
  • Cell Cycle / drug effects
  • Cell Division / drug effects
  • Cycloheximide / pharmacology
  • DNA Polymerase II / genetics
  • Dexamethasone / pharmacology*
  • G1 Phase / drug effects
  • G1 Phase / physiology*
  • Genes, fos / drug effects
  • Genes, jun / drug effects
  • Genes, myc / drug effects
  • Glioma
  • Humans
  • Ornithine Decarboxylase / genetics
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • RNA, Neoplasm / genetics
  • RNA, Neoplasm / isolation & purification
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / physiology*

Substances

  • RNA, Messenger
  • RNA, Neoplasm
  • Tumor Suppressor Protein p53
  • Dexamethasone
  • Cycloheximide
  • DNA Polymerase II
  • Ornithine Decarboxylase