Growth-regulatory mechanism of two human esophageal-cancer cell lines in protein-free conditions

Int J Cancer. 1993 Sep 30;55(3):364-70. doi: 10.1002/ijc.2910550304.

Abstract

We investigated the growth-regulatory mechanism of 2 esophageal squamous-cancer cell lines, TE2-NS and TE3-OS cells, both of which can grow stably in protein-free conditions in vitro. Protein-free conditioned media from TE2-NS and TE3-OS cells stimulated the growth of these cells. Exogenous epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), insulin-like growth factor (IGF)-I and -II enhanced cell proliferation by 2.2- to 3.8-fold in protein-free conditions, as compared with an untreated control. Receptor-binding assays showed that both TE2-NS and TE3-OS cells possessed a single class of high-affinity binding sites for IGF-I and 2 classes of binding sites for TGF-alpha, as confirmed on the cell membrane by immunochemistry. These results suggest that EGF, TGF-alpha and IGFs are candidates for the autocrine growth factor in cancer cells. The addition of inhibitory monoclonal antibodies against TGF-alpha and EGFR, but not those against either EGF or IGF-IR, significantly inhibited growth of the cells. Immunocytochemical staining and ELISA of the conditioned media both confirmed the production of TGF-alpha protein, but not EGF protein, in these cell lines. The data for a protein-free culture system strongly suggested that TGF-alpha, but not EGF or IGF, is biologically important as an autocrine growth factor in the growth of these cell lines in vitro.

MeSH terms

  • Antibodies, Monoclonal
  • Carcinoma, Squamous Cell / chemistry
  • Carcinoma, Squamous Cell / metabolism
  • Carcinoma, Squamous Cell / pathology*
  • Cell Division / drug effects
  • Culture Media, Serum-Free
  • Epidermal Growth Factor / metabolism
  • Epidermal Growth Factor / pharmacology
  • ErbB Receptors / analysis
  • ErbB Receptors / antagonists & inhibitors
  • ErbB Receptors / metabolism
  • Esophageal Neoplasms / chemistry
  • Esophageal Neoplasms / metabolism
  • Esophageal Neoplasms / pathology*
  • Humans
  • Insulin-Like Growth Factor I / metabolism
  • Insulin-Like Growth Factor I / pharmacology
  • Insulin-Like Growth Factor II / metabolism
  • Insulin-Like Growth Factor II / pharmacology
  • Receptor, IGF Type 1 / analysis
  • Receptor, IGF Type 1 / antagonists & inhibitors
  • Receptor, IGF Type 1 / metabolism
  • Transforming Growth Factor alpha / metabolism
  • Transforming Growth Factor alpha / pharmacology
  • Tumor Cells, Cultured

Substances

  • Antibodies, Monoclonal
  • Culture Media, Serum-Free
  • Transforming Growth Factor alpha
  • Epidermal Growth Factor
  • Insulin-Like Growth Factor I
  • Insulin-Like Growth Factor II
  • ErbB Receptors
  • Receptor, IGF Type 1