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[Cancer Research 59, 14-18, January 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 14-18, January 1, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Retinoid Receptor-dependent and -independent Effects of N-(4-Hydroxyphenyl)retinamide in F9 Embryonal Carcinoma Cells1

John L. Clifford2, David G. Menter, Michael Wang, Reuben Lotan and Scott M. Lippman

Departments of Clinical Cancer Prevention [J. L. C., D. G. M., M. W., S. M. L.] and Tumor Biology [R. L.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

Fenretinide {N-[4-hydroxyphenyl]retinamide (4HPR)} is a retinoid analogue with antitumor and chemopreventive activities. The mechanism of action of 4HPR is not fully understood, but it is hypothesized that this compound acts independently of the nuclear retinoid receptor pathway. To test this hypothesis directly, we have analyzed the activity of 4HPR on a panel of F9 embryonal carcinoma cell lines, which includes wild-type and mutant lines that lack expression of retinoic acid receptor {gamma}, retinoid X receptor {alpha}, or both. 4HPR (10 µM) treatment resulted in a rapid induction of cell death in F9 cells, which was responsible for their near elimination by 48 h. This effect occurred in the receptor-null cell lines as well. Treatment of the wild-type cells for 4 days with 1 µM 4HPR also resulted in a primitive endodermal differentiated phenotype that is normally seen upon all-trans-retinoic acid treatment and is characterized by the up-regulation of laminin B1 and type IV collagen. This differentiation response did not occur in the receptor-null cells. Therefore, two distinct effects of 4HPR were identified in this system: a rapid induction of cell death and a slower induction of differentiation, which are likely to be receptor independent and dependent, respectively.




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