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EGF and TGF‐α, the ligands of hyperproduced EGFR in human esophageal carcinoma cells, act as autocrine growth factors
Author(s) -
Yoshida Kazuhiro,
Kyo Eikai,
Tsuda Toshitaka,
Tsujino Tetsuhiro,
Ito Masanori,
Niimoto Minoru,
Tahara Elichi
Publication year - 1990
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910450124
Subject(s) - autocrine signalling , tgf alpha , epidermal growth factor , epidermal growth factor receptor , transforming growth factor , cancer research , biology , cell culture , cell growth , growth factor , microbiology and biotechnology , receptor , medicine , endocrinology , biochemistry , genetics
In order to ascertain autocrine growth factors in esophageal carcinomas, we analysed expression of mRNAs and proteins for epidermal growth factor (EGF), transforming growth factor‐α (TGF‐α) and epidermal growth factor receptor (EGFR) in 6 esophageal carcinoma cell lines. Gene alterations were also examined. All of the esophageal carcinoma cell lines expressed mRNA for EGFR and TGF‐α genes. Interestingly, EGF mRNA of about 5.0 kb was also detected in TE‐1, TE‐2, and TE‐8 cells. Production of protein was also confirmed by binding assay and ELISA on 3 of the 6 cell lines. The cells had a relatively high number of EGFRs and produced TGF‐α and EGF protein at the same time. Furthermore, anti‐EGF (KEM‐10) and anti‐TGF‐α (WA‐3) monoclonal antibodies (MAbs) inhibited spontaneous uptake of tritiated thymidine ( 3 H‐TdR) by TE‐1 cells which expressed EGF, TGF‐α and EGFR mRNA and protein. These results strongly suggest that EGF and/or TGF‐α produced by carcinoma cells function as autocrine growth factors for human esophageal carcinomas.