Induction of the c-jun proto-oncogene by a protein kinase C-dependent mechanism during exposure of human epidermal keratinocytes to ethanol

Biochem Pharmacol. 1993 Feb 9;45(3):675-81. doi: 10.1016/0006-2952(93)90142-j.

Abstract

The present work demonstrates that ethanol induces expression of the c-jun proto-oncogene in human keratinocytes. Increased c-jun mRNA levels were detectable at 1 hr of exposure to 1% ethanol and at 24 hr remained above that in control keratinocytes. An increase in c-jun expression was also detectable at ethanol concentrations of 0.1 and 0.5%. Similar findings were obtained for the related jun-B and c-fos early response genes. The results also demonstrate that ethanol exposure is associated with increases in protein kinase C activity in both the cytosol and membrane fractions. This increase was detectable at 5 min and maximal at 30-60 min. The finding that induction of c-jun expression by ethanol was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggested that this effect is mediated by protein kinase C. Furthermore, down-regulation of protein kinase C by prolonged exposure to 12-O-tetradecanoylphorbol-13-acetate was associated with a block in ethanol-induced c-jun expression. We also demonstrated that ethanol exposure is associated with rapid (5-30 min) increases in intracellular levels of diradylglycerol. Taken together, these findings demonstrate that the exposure of keratinocytes to ethanol results in the activation of protein kinase C and c-jun expression.

Publication types

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

MeSH terms

  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • Cells, Cultured
  • Diglycerides / analysis
  • Dose-Response Relationship, Drug
  • Enzyme Activation / drug effects
  • Ethanol / pharmacology*
  • Gene Expression / drug effects
  • Humans
  • Isoquinolines / pharmacology
  • Keratinocytes / drug effects*
  • Keratinocytes / metabolism
  • Piperazines / pharmacology
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism*
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins c-jun / biosynthesis*
  • Proto-Oncogenes*
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / isolation & purification
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Diglycerides
  • Isoquinolines
  • MAS1 protein, human
  • Piperazines
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins c-jun
  • RNA, Messenger
  • Ethanol
  • diarachidonyl diglyceride
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate