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Modulation of Epidermal Growth Factor Receptors by Retinoic Acid in ME180 Cells¹

Department of Dermatology, University of Rochester Medical Center, Rochester, New York 14642

Retinoic acid (RA) increases epidermal growth factor (EGF) receptors in many cells; in ME180 cells, a human epidermoid carcinoma, RA resulted in a dose- and time-dependent reduction of EGF binding. In RA-treated ME180 cells, binding was 41% of the control. The reduction of EGF binding was due to a decrease in the number of receptors, from 8.7 x 10⁴ to 3.6 x 10⁴ per cell. The difference was present 8 h after the addition of RA and was reversible 3 days after its removal. Scatchard analysis indicated that RA did not change the binding affinity of EGF (K_d = 1 nM). Also, RA did not alter the rate of EGF internalization or the down-regulation induced by exogenous EGF. Flow-cytometric analysis revealed that RA did not alter the cell cycle. Soluble cell membrane extracts were prepared in a Tris buffer with protease inhibitors, immunoprecipitated, electrophoresed, and immunoblotted with an antiserum to EGF receptors. The EGF receptor band of M_r 170,000 was decreased in RA-treated cells. These results suggest that RA reduces the synthesis of EGF receptors in ME180 cells.

¹ Supported by USPHS Grants AR30126 and AR30965. Presented in part at the Society for Investigative Dermatology annual meeting, May, 1988 (J. Invest. Dermatol., 90: 620, 1988).

² To whom requests for reprints should be addressed, at University of Rochester Medical Center, 601 Elmwood Avenue, P.O. Box 697, Rochester, NY 14642.

Received 3/29/89. Revised 9/28/89. Accepted 11/ 9/89.

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