Targeted disruption of β1-integrin in a transgenic mouse model of human breast cancer reveals an essential role in mammary tumor induction

被引:362
作者
White, DE
Kurpios, NA
Zuo, DM
Hassell, JA
Blaess, S
Mueller, U
Muller, WJ [1 ]
机构
[1] Royal Victoria Hosp, Mol Oncol Grp, Montreal, PQ H3A 1A1, Canada
[2] McMaster Univ, Dept Med Sci, Hamilton, ON L8S 4K1, Canada
[3] McMaster Univ, Dept Biochem, Hamilton, ON L8S 4K1, Canada
[4] NYU, Sch Med, Howard Hughes Med Inst, New York, NY 10016 USA
[5] NYU, Sch Med, Skirball Inst Biomol Med, Dev Genet Program, New York, NY 10016 USA
[6] Scripps Res Inst, Dept Cell Biol, La Jolla, CA 92037 USA
[7] McGill Univ, Dept Med, Montreal, PQ H3A 1A1, Canada
[8] McGill Univ, Dept Biochem, Montreal, PQ H3A 1A1, Canada
基金
美国国家卫生研究院; 加拿大健康研究院;
关键词
D O I
10.1016/j.ccr.2004.06.025
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Despite evidence demonstrating the role of beta1-integrin in the regulation of cancer cell proliferation in vitro, the importance of this cell adhesion receptor during the initiation and progression of epithelial tumors in vivo remains unclear. Here we have used the Cre/LoxP1 recombination system to disrupt beta1-integrin function in the mammary epithelium of a transgenic mouse model of human breast cancer. Using this approach, we show that beta1-integrin expression is critical for the initiation of mammary tumorigenesis in vivo, and for maintaining the proliferative capacity of late-stage tumor cells. These observations provide a direct demonstration that beta1-integrin plays a critical role in both the initiation and maintenance of mammary tumor growth in vivo.
引用
收藏
页码:159 / 170
页数:12
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