Mammalian lignans enterolactone and enterodiol, alone and in combination with the isoflavone genistein, do not promote the growth of MCF-7 xenografts in ovariectomized athymic nude mice

Authors

  • Krista A. Power,

    1. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
    Search for more papers by this author
  • Niina M. Saarinen,

    1. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
    Current affiliation:
    1. Functional Foods Forum and Institute of Biomedicine, University of Turku, Kiinamyllynkatu 10, FIN-20520, Turku, Finland
    Search for more papers by this author
  • Jian Min Chen,

    1. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
    Search for more papers by this author
  • Lilian U. Thompson

    Corresponding author
    1. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
    • Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, 150 College St., Toronto, Ontario, Canada M5S 3E2
    Search for more papers by this author
    • Fax: +416 978-5882


Abstract

This study determined the effect of the mammalian lignans enterolactone (ENL) and enterodiol (END) alone and in combination with the isoflavone genistein (GEN) on the growth of MCF-7 tumors in ovariectomized nude mice. Ovariectomized athymic nude mice with established MCF-7 tumors were fed a basal diet (AIN-93G) and divided into 5 groups that received daily subcutaneous injections (10 mg/kg body weight (BW)) of ENL, END, GEN, a mixture of these compounds (MIX), or vehicle as a negative control for 22 weeks. A positive control group was implanted with an estradiol pellet in order to establish an estrogenic tumor growth response. In the ENL- and END-treated mice, palpable tumors regressed significantly by 91 and 83%, respectively, resulting in final tumors that were similar to the negative control tumors. However, tumor cell apoptosis was significantly enhanced by the lignans. In the GEN-treated mice, tumors initially regressed significantly by 64% but regression ceased following prolonged treatment, resulting in final tumors that were significantly larger compared to negative control, ENL-, and END-treated mice, in part by increasing tumor cell proliferation. The MIX treatment significantly regressed palpable tumors by 87% similar to negative control group, with no effects on tumor cell apoptosis or proliferation. The isoflavone GEN alone promoted the growth of established MCF-7 human breast cancer xenografts after prolonged treatment while the mammalian lignans ENL and END did not. When these phytoestrogens were given in combination, no tumor growth-promoting effects were observed. © 2005 Wiley-Liss, Inc.

Ancillary