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[Cancer Research 52, 4766-4772, September 1, 1992]
© 1992 American Association for Cancer Research

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Differential Susceptibility of Cultured Human Melanoma Cell Lines to Enhancement by Retinoic Acid of Intercellular Adhesion Molecule 1 Expression1

Zhigang Wang, Yan Cao, Claudio M. D'Urso and Soldano Ferrone2

Department of Microbiology and Immunology, New York Medical College, Valhalla, New York 10595

The potential role of intercellular adhesion molecule 1 (ICAM-1) in the biology of human melanoma cells has stimulated interest in the characterization of its modulation. The present study has shown that the differentiating agent retinoic acid (RA) up-regulates ICAM-1 expression by melanoma cells in a dose- and time-dependent fashion. The enhancement of ICAM-1 cell surface expression is paralleled by an increase in ICAM-1 mRNA. Therefore, ICAM-1 represents an additional gene which may be transcriptionally regulated by RA. The five melanoma cell lines tested displayed a differential susceptibility to the modulation of ICAM-1 expression by RA, since the cell line MeWo did not change in its ICAM-1 expression following incubation with RA. Nevertheless, RA-insensitive as well as RA-sensitive melanoma cell lines displayed a higher increase in ICAM-1 expression following incubation with RA and cytokines than following incubation with each of them. Analysis of the distribution in the melanoma cell lines of retinoic acid receptors (RARs) showed a relationship between susceptibility to a RA-mediated increase of ICAM-1 expression and RARß expression, suggesting that the latter receptor may play a role in the phenomenon. RAR{alpha} and RAR{gamma} were present in RA-sensitive and -insensitive melanoma cell lines, suggesting that they play a role in the enhancement by RA of cytokine-mediated up-regulation of ICAM-1 expression. The melanoma cell lines we have described may represent a useful system for investigating the role of RAR in the regulation of gene expression and the mechanism(s) which underlie this effect.

1 Supported by USPHS Grants CA37959 and CA39559 awarded by the National Cancer Institute, Department of Health and Human Services.

2 To whom requests for reprints should be addressed.

Received 3/13/92. Accepted 6/22/92.




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Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1992 by the American Association for Cancer Research.