Cell growth inhibition by prostaglandin A2 results in elevated expression of gadd153 mRNA. Academic Article uri icon

Overview

MeSH

  • 2-Aminopurine
  • Base Sequence
  • Blotting, Northern
  • Cycloheximide
  • DNA Damage
  • Dactinomycin
  • HeLa Cells
  • Humans
  • Kinetics
  • Molecular Sequence Data

MeSH Major

  • Cell Division
  • Gene Expression Regulation
  • Prostaglandins A
  • RNA, Messenger

abstract

  • Treatment of Hela cells with prostaglandin A2 (PGA2) resulted in a marked inhibition of cell proliferation which was associated with a significant induction of gadd153 mRNA, a member of a novel class of genes associated with growth arrest and DNA damage. Induction of gadd153 mRNA was specific to prostaglandins capable of arresting cell growth and was dose-dependent with the maximum effect seen at 36 microM PGA2. Induction was rapid, occurring within 2-4 h and reaching a maximum by 8 h. These effects were reversible as removal of PGA2 resulted in a rapid decline in gadd153 mRNA levels coincident with resumption of cell growth. PGA2 induction of gadd153 mRNA was completely prevented by the presence of actinomycin D at a concentration sufficient to block transcription and was partially inhibited (50%) by the protein synthesis inhibitor cycloheximide. The presence of the protein kinase inhibitor 2-aminopurine decreased the PGA2 induction of gadd153 mRNA by greater than 90%, suggesting that cellular kinases play a role in the induction of gadd153 by PGA2. Thus PGA2-mediated growth arrest provides a useful model to further define the role of gadd153 in the negative control of cell growth.

publication date

  • March 1992

has subject area

  • 2-Aminopurine
  • Base Sequence
  • Blotting, Northern
  • Cell Division
  • Cycloheximide
  • DNA Damage
  • Dactinomycin
  • Gene Expression Regulation
  • HeLa Cells
  • Humans
  • Kinetics
  • Molecular Sequence Data
  • Prostaglandins A
  • RNA, Messenger

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed ID

  • 1735464

Additional Document Info

start page

  • 85

end page

  • 89

volume

  • 199

number

  • 1