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Estrogen Induces Lung Metastasis through a Host Compartment–Specific Response

Division of Cancer and Vascular Biology, La Jolla Institute for Molecular Medicine, San Diego, California

Requests for reprints: Brian P. Eliceiri, Division of Cancer and Vascular Biology, La Jolla Institute for Molecular Medicine, 4570 Executive Drive, Suite #100, San Diego, CA 92121. Phone: 858-587-8788; Fax: 858-587-6742; E-mail: beliceiri{at}ljimm.org.

Direct proliferative effects of estrogen (E₂) on estrogen receptor–positive tumors are well documented; however, the potential for E₂ to mediate effects selective for the host (i.e., angiogenesis, vascular permeability, or stromal effects), which influence tumor growth and/or metastasis, has received less attention. In this study, we examine the capacity for E₂ to promote tumor growth and/or metastasis independent of direct effects on tumor cells. In these studies, we distinguish host versus tumor compartment components of E₂ action in tumor growth and metastasis by analysis of E₂-nonresponsive tumor cells implanted in ovariectomized (OVX) mice that contain s.c. implants of placebo (OVX) or E₂-containing slow-release pellets (OVX + E₂). We show that the D121 lung carcinoma cell line is E₂-nonresponsive, and following s.c. implantation in OVX versus OVX + E₂ mice, E₂ action on the host compartment leads to an increase in spontaneous metastasis but not primary tumor growth or neovascularization. Similarly, experimental lung metastasis of E₂-nonresponsive 4T1 mammary carcinoma cells also leads to increased tumor burden in the lungs of OVX + E₂ mice. These results suggest that the E₂ status of the host compartment influences late steps in tumor cell metastasis that can provide important insights into the role of E₂ in the tumor versus host compartments. (Cancer Res 2006; 66(7): 3667-72)

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