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Overexpression of Epidermal Growth Factor and Insulin-like Growth Factor-I Receptors and Autocrine Stimulation in Human Esophageal Carcinoma Cells¹

Graduate Institute of Microbiology and Immunology, National Yang-Ming Medical College [S-C. C., C-K. C., F-H. W., C. C., C-p. H.]; Department of Medical Research, Veterans General Hospital [C-K. C., C. C., C-p. H.]; and Institute of Biomedical Sciences, Academia Sinica [S-C. C.], Taipei, Taiwan, Republic of China

The growth-stimulatory effects of epidermal growth factor (EGF), transforming growth factor (TGF-), and insulin-like growth factor-I (IGF-I) on the human esophageal carcinoma cell line CE48T/VGH were evaluated. Under serum-free conditions, EGF, TGF-, and IGF-I promoted 3.6- to 4.1-fold increased cell proliferation. Scatchard analyses and Northern blot hybridization revealed that both the EGF/TGF- receptor and the IGF-I receptor were overexpressed in CE48T/VGH cells. Furthermore, ligand-dependent autophosphorylation of the EGF receptor and the IGF-I receptor was clearly detected using antireceptor and antiphosphotyrosine antibodies. Autocrine regulation was strongly indicated by the following evidence: (a) CE48T/VGH cells were found to express TGF- and IGF-I genes, (b) serum-free conditioned medium promoted the growth of CE48T/VGH cells and stimulated the autophosphorylation of the EGF/TGF- receptor and the IGF-I receptor, and (c) the addition of IGF-I receptor antibodies significantly suppressed CE48T/VGH cell growth under serum-free conditions. Our studies suggest that the overexpression of EGF and IGF-I receptors and autocrine growth regulation may concertedly control the proliferation of esophageal carcinoma cells.

¹ This work was supported by Grant NSC79-0412-B075-37 from the National Science Council, Republic of China.

² To whom requests for reprints should be addressed.

Received 9/ 4/90. Accepted 1/21/91.

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