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Experimental Therapeutics

Comparison of N-(4-hydroxyphenyl)retinamide and all-trans-Retinoic Acid in the Regulation of Retinoid Receptor-mediated Gene Expression in Human Breast Cancer Cell Lines

Syed M. I. Kazmi, Richard K. Plante, Vito Visconti and Catherine Y. Lau
Syed M. I. Kazmi
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Richard K. Plante
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Vito Visconti
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Catherine Y. Lau
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DOI:  Published March 1996
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Abstract

The activities of N-(4-hydroxyphenyl)retinamide [(4-HPR), Fenretinide] and all-trans-retinoic acid (RA) were determined for (a) the inhibition of cell proliferation; (b) the activation of human retinoid receptor-mediated target gene expression; (c) the inhibition of estradiol- and progesterone-induced gene activation in breast cancer cell lines; and (d) the regulation of the expression of tumor suppressor retinoblastoma protein. Similar to RA, both 4-HPR and its active metabolite N-(4-methoxyphenyl)retinamide (4-MPR) effectively impeded the growth of MCF7 and T-47D human breast cancer cell lines, except that 4-HPR also inhibited the proliferation of RA-resistant BT-20 cells. However, when tested in human recombinant retinoic acid receptor (RAR-α, RAR-β, and RAR-γ)-induced reporter gene assays, RA was much more potent (>100-fold) than either 4-HPR or 4-MPR. 4-HPR induced transcriptional activation through all three RAR subtypes at 1–10 µm, while RA showed comparable activity at 10–100 nm. Despite the apparent weak interaction at the RAR level, 4-HPR was comparable to RA in the inhibition of both estrogen receptor- and progesterone receptor-mediated transcriptional activation in MCF7 and T-47D cells, respectively. Moreover, similar to RA, 4-HPR and 4-MPR caused marked up-regulation of tumor suppressor retinoblastoma protein in both MCF7 and T-47D cells. Since RA and 4-HPR showed comparable activity in the inhibition of estrogen receptor- and progesterone receptor-induced gene transcription and in the stimulation of retinoblastoma protein expression in MCF7 and T-47D cells, the reduced RAR activation by 4-HPR may result in the lack of hepatic toxicity and therefore the improved therapeutic efficacy relative to RA.

Footnotes

  • ↵1 To whom requests for reprints should be addressed.

  • Received May 8, 1995.
  • Accepted January 3, 1996.
  • ©1996 American Association for Cancer Research.
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March 1996
Volume 56, Issue 5
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Comparison of N-(4-hydroxyphenyl)retinamide and all-trans-Retinoic Acid in the Regulation of Retinoid Receptor-mediated Gene Expression in Human Breast Cancer Cell Lines
Syed M. I. Kazmi, Richard K. Plante, Vito Visconti and Catherine Y. Lau
Cancer Res March 1 1996 (56) (5) 1056-1062;

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Comparison of N-(4-hydroxyphenyl)retinamide and all-trans-Retinoic Acid in the Regulation of Retinoid Receptor-mediated Gene Expression in Human Breast Cancer Cell Lines
Syed M. I. Kazmi, Richard K. Plante, Vito Visconti and Catherine Y. Lau
Cancer Res March 1 1996 (56) (5) 1056-1062;
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