Sulforaphane prevents mouse skin tumorigenesis during the stage of promotion

被引:95
作者
Gills, Joell J.
Jeffery, Elizabeth H.
Matusheski, Nathan V.
Moon, Richard C.
Lantvit, Daniel D.
Pezzuto, John M.
机构
[1] Purdue Univ, Coll Pharm Nursing & Hlth Sci, W Lafayette, IN 47907 USA
[2] Univ Illinois, Dept Med Chem & Pharmacognosy, Chicago, IL 60612 USA
[3] Univ Illinois, Dept Food Sci & Human Nutr, Urbana, IL 61801 USA
[4] Kraft Foods, Northfield, IL 60093 USA
关键词
sulforaphane; isothiocyanate; ornithine decarboxylase; 7,12-dimethylbenz(a)anthracene; 12-O-tetradecanoylphorbol; 13-acetate;
D O I
10.1016/j.canlet.2005.05.007
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Sulforaphane (SF), a natural product from broccoli, is known to enhance detoxification of carcinogens and block initiation of chemically-induced carcinogenesis in animal models. Cell culture and xenograft studies suggest additional roles for SF, inhibiting growth of tumors, arresting the cell cycle and enhancing apoptosis. As currently reported, topical SF (1, 5 or 10 mu mol/mouse) significantly inhibited 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol 13-acetate (TPA)-induced mouse skin tumorigenesis, using either an anti-promotion protocol (SF from 1 week after carcinogen until the end of the study) or a combined anti-initiation, anti-promotion protocol (SF 7 days prior to carcinogen until the end of the study). Surprisingly, no significant effect was observed in an anti-initiation protocol (SF from 7 days prior to 7 days after carcinogen). Separately, SF inhibited TPA-induced ornithine decarboxylase activity in mouse skin, an obligate step in TPA-induced promotion of carcinogenesis. These data link this molecular mechanism to SF-dependent inhibition of the promotion of tumorigenesis. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:72 / 79
页数:8
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