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[Cancer Research 48, 2377-2381, May 1, 1988]
© 1988 American Association for Cancer Research

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Isolation and Characterization of A-431 Cells That Retain High Epidermal Growth Factor Binding Capacity and Respond to Epidermal Growth Factor by Growth Stimulation1

Angie Rizzino2, Eric Ruff and Peter Kazakoff

Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska 68105

A-431 cells, which exhibit large numbers of epidermal growth factor (EGF) receptors and respond to EGF by growth inhibition, are widely used to study EGF receptors and the effects of EGF. In this report, we describe the isolation and characterization of variant A-431 cells that respond to EGF by growth stimulation. One variant, which is referred to as A-431R-1, has been characterized in detail. EGF stimulates both monolayer and soft agar growth of A-431R-1 cells cultured in serum-free medium. In contrast to the original A-431 cells, growth of A-431R-1 cells is not inhibited by EGF, even at high concentrations. Scatchard analysis of EGF binding to A-431R-1 cells and A-431 cells indicates that both cell populations exhibit approximately 1.8 x 106 EGF receptors per cell. Thus, unlike other variants of A-431 cells that are not inhibited by EGF, A-431R-1 cells exhibit as many EGF receptors as the parental A-431 cells. It was also determined that the phorbol ester 12-O-tetradecanoylphorbol-13-acetate reduces EGF binding to the high affinity receptors of A-431R-1 cells; whereas, transforming growth factor type ß did not significantly affect EGF binding. Our results suggest that A-431R-1 cells should be useful for studying the biochemical effects of EGF and for examining why some cells are inhibited by EGF, whereas others are stimulated by EGF.

1 Supported by grants from the National Institutes of Health (HD 21568), the Nebraska Department of Health (86-11R and 87-38), and the National Cancer Institute (Laboratory Cancer Research Center Support Grant CA 36727).

2 To whom requests for reprints should be addressed.

Received 8/18/87. Revised 12/15/87. Accepted 1/28/88.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1988 by the American Association for Cancer Research.