Transcriptional activation of c-fos and c-jun protooncogenes by serum growth factors in osteoblast-like MC3T3-E1 cells

J Bone Miner Res. 1992 Oct;7(10):1149-55. doi: 10.1002/jbmr.5650071006.

Abstract

The present study was undertaken to clarify the relationship between c-fos and c-jun protooncogene expression and the differentiation and/or proliferation of osteoblasts, using osteoblast-like MC3T3-E1 (E1) cells. c-fos mRNA was barely detectable, whereas c-jun mRNA was constitutively expressed in E1 cells after serum deprivation for 24-72 h. When serum was added, a rapid and transient induction of c-fos and c-jun mRNAs was observed. The c-fos and c-jun mRNAs reached peak levels at 30 minutes, with a rapid disappearance of c-fos mRNA within 3 h and a much slower decrease in c-jun mRNA. The addition of serum together with cycloheximide, an inhibitor of protein synthesis, resulted in the superinduction of both c-fos and c-jun mRNAs. Among various growth factors, PDGF, EGF, and bFGF mimicked the serum effect, whereas IGF-I and TGF-beta failed to induce c-fos and c-jun mRNA. The effects of PDGF, EGF, and bFGF were completely abolished by pretreatment with actinomycin D, an inhibitor of RNA synthesis, suggesting a transcriptional mechanism. Nuclear runoff experiments showed that the transcription rate of c-fos and c-jun protooncogenes was increased by serum and growth factors. The effects of PDGF, EGF, and bFGF were inhibited by H-7 or staurosporine, inhibitors of protein kinase C (PKC), but not by HA1004 with a much weaker inhibitory activity, suggesting the involvement of PKC for the activation of the protooncogenes.(ABSTRACT TRUNCATED AT 250 WORDS)

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • 3T3 Cells
  • Alkaloids / pharmacology
  • Animals
  • Cell Differentiation / drug effects
  • Cycloheximide / pharmacology
  • Dactinomycin / pharmacology
  • Epidermal Growth Factor / pharmacology
  • Fibroblast Growth Factor 2 / pharmacology
  • Gene Expression Regulation / drug effects*
  • Growth Substances / pharmacology*
  • Insulin-Like Growth Factor I / pharmacology
  • Isoquinolines / pharmacology
  • Mice
  • Osteoblasts / cytology
  • Osteoblasts / metabolism*
  • Piperazines / pharmacology
  • Platelet-Derived Growth Factor / pharmacology
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-jun / genetics
  • Proto-Oncogenes*
  • RNA, Messenger / metabolism
  • Staurosporine
  • Transforming Growth Factor beta / pharmacology

Substances

  • Alkaloids
  • Growth Substances
  • Isoquinolines
  • Piperazines
  • Platelet-Derived Growth Factor
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins c-fos
  • Proto-Oncogene Proteins c-jun
  • RNA, Messenger
  • Transforming Growth Factor beta
  • Fibroblast Growth Factor 2
  • Dactinomycin
  • Epidermal Growth Factor
  • Insulin-Like Growth Factor I
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • Cycloheximide
  • Staurosporine