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17β-Estradiol Mobilizes Bone Marrow–Derived Endothelial Progenitor Cells to Tumors

¹ Department of Microbiology and Immunology, New York Medical College, Valhalla, New York and ² Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois

Requests for reprints: Raj K. Tiwari, Department of Microbiology and Immunology, New York Medical College, Valhalla, NY 10595. Phone: 914-594-4870; Fax: 914-594-4879; E-mail: raj_tiwari{at}nymc.edu and Raj Kishore, Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Chicago, IL 60611. Phone: 312-503-1651; E-mail: r-kishore{at}northwestern.edu.

Key Words: Tumor biology • breast cancer • cell mobilization • progenitor endothelial cells • conditioned media

Neovascularization is critical for tumor growth and development. The cellular mediators for this process are yet to be defined. We discovered that bone marrow–derived endothelial progenitor cells (BM-EPC), having the phenotype (CD133+, CD34+, VEGFR-2+), initiate neovascularization in response to TG1-1 mammary cells implanted in the inguinal mammary gland of Tie-2 GFP transgenic mice. The fluorescence tag allowed for tracing the migration of green fluorescent protein–tagged endothelial progenitor cells to tumor tissues. We discovered that 17-β estradiol supplementation of ovariectomized mice significantly enhanced BM-EPC–induced neovascularization and secretion of angiogenic factors within the tumor microenvironment. Cell-based system analyses showed that estrogen-stimulated BM-EPCs secreted paracrine factors which enhanced TG1-1 cell proliferation and migration. Furthermore, TG1-1 cell medium supplemented with estrogen-induced BM-EPC mediated tubulogenesis, which was an experimental in vivo representation of the neovasculature. Our data provide evidence of BM-EPC mammary tumor cell interactions and identify a novel cellular mediator of tumor progression that can be exploited clinically. [Cancer Res 2008;68(15):6038–42]

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