Amplification and expression of the TGF-alpha, EGF receptor and c-myc genes in four human oesophageal squamous cell carcinoma lines

Biosci Rep. 1993 Oct;13(5):303-12. doi: 10.1007/BF01137967.

Abstract

We have previously shown that four human oesophageal squamous cell carcinoma (SCC) cell lines secrete significant quantities of transforming growth factor alpha (TGF-alpha) in vitro. Three of these lines are known to produce supernumerary low-affinity epidermal growth factor receptors (EGF-Rs). Using an 125I-EGF competitive binding assay and Scatchard analysis, we show that the fourth also overproduces low-affinity receptors. According to slot blot DNA analyses, the secretion of high levels of TGF-alpha is not associated with amplification of the TGF-alpha gene, and hyperproduction of the EGF-R is correlated with receptor gene amplification. Western blot analyses show that the c-Myc protein is overexpressed in two of the cell lines; and Southern and Northern blot analyses indicate that this overexpression occurs independently of c-myc gene amplification. Our results are consistent with an autocrine role for TGF-alpha and EGF-R in oesophageal carcinogenesis and support the possibility that c-myc overexpression may be required for the in vivo tumourigenicity of cells that produce high levels of TGF-alpha and the EGF-R.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology
  • Carcinoma, Squamous Cell / genetics*
  • Carcinoma, Squamous Cell / metabolism
  • Carcinoma, Squamous Cell / pathology
  • Colonic Neoplasms / genetics
  • Colonic Neoplasms / metabolism
  • Colonic Neoplasms / pathology
  • ErbB Receptors / biosynthesis
  • ErbB Receptors / genetics*
  • ErbB Receptors / physiology
  • Esophageal Neoplasms / genetics*
  • Esophageal Neoplasms / metabolism
  • Esophageal Neoplasms / pathology
  • Gene Amplification*
  • Gene Expression Regulation, Neoplastic*
  • Genes, myc*
  • Humans
  • Neoplasm Proteins / biosynthesis*
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism
  • Transforming Growth Factor alpha / biosynthesis
  • Transforming Growth Factor alpha / genetics*
  • Transforming Growth Factor alpha / physiology
  • Tumor Cells, Cultured

Substances

  • Neoplasm Proteins
  • Transforming Growth Factor alpha
  • ErbB Receptors