PACAP stimulates transcription of c-Fos and c-Jun and activates the AP-1 transcription factor in rat pancreatic carcinoma cells

Biochem Biophys Res Commun. 1996 Apr 5;221(1):111-6. doi: 10.1006/bbrc.1996.0554.

Abstract

Pituitary Adenylate Cyclase Activating Peptide (PACAP) strongly induces proliferation of the rat pancreatic carcinoma cell line AR4-2J via interaction with the G-protein coupled type 1 PACAP/VIP (PVI) receptor. RT-PCR analysis revealed that this mitogenic effect of PACAP is preceded by a rapid and transient increase of transcription of the protooncogene c-fos and to a lesser extent of c-jun. Transcriptional activation is abolished by a specific PACAP antagonist and by inhibitors of PKC and PKA. In parallel to c-fos/c-jun induction, PACAP rapidly activates the heterodimeric transcription factor AP-1, as shown by electrophoretic mobility shift assay. These findings demonstrate that signal transduction of a growth-stimulating G-protein-coupled receptor involves the c-fos/c-jun/AP-1 cascade, a pathway mainly linked to classical growth factor receptor tyrosine kinases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • DNA Primers
  • Molecular Sequence Data
  • Neuropeptides / pharmacology*
  • Pancreatic Neoplasms / metabolism*
  • Pancreatic Neoplasms / pathology
  • Pituitary Adenylate Cyclase-Activating Polypeptide
  • Proto-Oncogene Proteins c-fos / genetics*
  • Proto-Oncogene Proteins c-jun / genetics*
  • Rats
  • Signal Transduction
  • Transcription Factor AP-1 / metabolism*
  • Transcription, Genetic / drug effects*
  • Tumor Cells, Cultured

Substances

  • Adcyap1 protein, rat
  • DNA Primers
  • Neuropeptides
  • Pituitary Adenylate Cyclase-Activating Polypeptide
  • Proto-Oncogene Proteins c-fos
  • Proto-Oncogene Proteins c-jun
  • Transcription Factor AP-1