Transcriptional regulation of the transforming growth factor beta 1 promoter by v-src gene products is mediated through the AP-1 complex

Mol Cell Biol. 1990 Sep;10(9):4978-83. doi: 10.1128/mcb.10.9.4978-4983.1990.

Abstract

Growth factor-independent 32D-src and 32D-abl cell lines, established by infecting the interleukin-3-dependent myeloid precursor cell line (32D-123) with retroviruses containing the src or abl oncogene, were used to study transcriptional regulation of transforming growth factor beta 1 (TGF-beta 1) mRNA. Analysis of different TGF-beta 1 promoter constructs regulated by pp60v-src indicated that sequences responsive to high levels of src induction contain binding sites for AP-1. Both src and serum induced expression of the c-fos and c-jun genes in myeloid cells, resulting in transcriptional activation of the TGF-beta 1 gene. We found that serum treatment increased TGF-beta 1 mRNA levels in 32D-123 cells and that the v-Src protein could replace the serum requirement by stimulating binding to the AP-1 complex of the TGF-beta 1 promoter, thereby mediating the induction of TGF-beta 1 transcription.

Publication types

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

MeSH terms

  • Animals
  • Base Sequence
  • Cell Line
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Gene Expression Regulation*
  • Mice
  • Molecular Sequence Data
  • Oligonucleotide Probes
  • Oncogene Protein pp60(v-src) / metabolism*
  • Plasmids
  • Promoter Regions, Genetic*
  • Protein-Tyrosine Kinases / metabolism*
  • Proto-Oncogene Proteins c-jun
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transcription, Genetic*
  • Transforming Growth Factors / genetics*

Substances

  • DNA-Binding Proteins
  • Oligonucleotide Probes
  • Proto-Oncogene Proteins c-jun
  • Transcription Factors
  • Transforming Growth Factors
  • Protein-Tyrosine Kinases
  • Oncogene Protein pp60(v-src)