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Journal of Pharmacology and Experimental Therapeutics

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OtherCHEMOTHERAPY/GENE THERAPY

The Protective Effect of Metallothionein Against Lipid Peroxidation Caused by Retinoic Acid in Human Breast Cancer Cells

Darin Hurnanen, Hing Man Chan and Stan Kubow
Journal of Pharmacology and Experimental Therapeutics December 1997, 283 (3) 1520-1528;
Darin Hurnanen
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Hing Man Chan
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Stan Kubow
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Abstract

The treatment of breast cancer by retinoic acid (RA) may be mediated by lipid peroxidation. Expression of metallothionein (MT) in cancer cells, however, can protect against lipid peroxidation by scavenging hydroxyl radicals. In this study, a two-by-six factorial design was used to investigate the interactive effects of all-trans-RA and zinc (Zn)-induced MT on the growth of two human breast cancer cell lines differing in basal expression of MT and estrogen receptors; MCF7 cells express estrogen receptor, BT-20 cells do not. Cells were treated with Zn to induce MT and then treated with six RA concentrations. Cell proliferation, lipid peroxidation, MT protein, MT mRNA and glutathione concentrations were measured. BT-20 cells expressed higher constitutive MT concentrations than MCF7 cells. MT was significantly increased by Zn treatment in BT-20 cells but not in MCF7 cells. Low RA concentrations stimulated growth proliferation but higher concentrations inhibited cell proliferation. Elevated RA concentrations increased lipid peroxidation as measured by thiobarbituric acid reactive substances. There was a significant negative correlation between lipid peroxidation and cell proliferation. Growth inhibition and lipid peroxidation were reduced by Zn pretreatment in BT-20 cells but not in MCF7 cells. RA increased MT levels in both cell lines, which suggests that RA may generate free radicals which will induce MT mRNA expression. Glutathione did not appear to be a significant factor. Therefore, induction of MT by Zn may modulate the growth inhibitory effects of RA in human breast cancer cells. One mechanism of growth inhibition may be through increased lipid peroxidation. Induction of MT by RA may be one explanation for acquired RA resistance in cancer.

Footnotes

  • Send reprint requests to: Hing Man Chan, Centre for Indigenous Peoples’ Nutrition and Environment, Department of Dietetics and Human Nutrition, McGill University, 21,111 Lakeshore Road, Ste. Anne de Bellevue, Quebec, Canada H9X 3V9.

  • ↵1 Research funded by National Science and Engineering Research Council of Canada.

  • Abbreviations:
    atRA
    all-trans retinoic acid
    ER
    estrogen receptor
    GSH
    glutathione
    MT
    metallothionein
    PUFA
    polyunsaturated fatty acid
    RA
    retinoic acid
    TBARS
    thiobarbituric acid reactive substances
    Zn
    zinc
    ELISA
    enzyme-linked immunosorbent assay
    ANOVA
    analysis of variance
    • Received January 7, 1997.
    • Accepted August 11, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 283, Issue 3
1 Dec 1997
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OtherCHEMOTHERAPY/GENE THERAPY

The Protective Effect of Metallothionein Against Lipid Peroxidation Caused by Retinoic Acid in Human Breast Cancer Cells

Darin Hurnanen, Hing Man Chan and Stan Kubow
Journal of Pharmacology and Experimental Therapeutics December 1, 1997, 283 (3) 1520-1528;

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OtherCHEMOTHERAPY/GENE THERAPY

The Protective Effect of Metallothionein Against Lipid Peroxidation Caused by Retinoic Acid in Human Breast Cancer Cells

Darin Hurnanen, Hing Man Chan and Stan Kubow
Journal of Pharmacology and Experimental Therapeutics December 1, 1997, 283 (3) 1520-1528;
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