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

• Published in: International journal of cancer Vol. 55; no. 3; p. 364
• Main Authors: Iihara, K, Shiozaki, H, Oku, K, Tahara, H, Doki, Y, Oka, H, Kadowaki, T, Iwazawa, T, Inoue, M, Mori, T
• Format: Journal Article
• Language: English
• Published: United States 30-09-1993
• Subjects: 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
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910550304

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.