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Host CXCR2-Dependent Regulation of Melanoma Growth, Angiogenesis, and Experimental Lung Metastasis

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska

Requests for reprints: Rakesh K. Singh, Department of Pathology and Microbiology, University of Nebraska Medical Center, 985845 Nebraska Medical Center, Omaha, NE 68198-5845. Phone: 402-559-9949; Fax: 402-559-4077; E-mail: rsingh{at}unmc.edu.

Key Words: CXCR2 • Melanoma • Metastasis

Crucial steps in tumor growth and metastasis are proliferation, survival, and neovascularization. Previously, we have shown that receptors for CXCL-8, CXCR1, and CXCR2 are expressed on endothelial cells and CXCR2 has been shown to be a putative receptor for angiogenic chemokines. In this report, we examined whether tumor angiogenesis and growth of CXCL-8–expressing human melanoma cells are regulated in vivo by a host CXCR2–dependent mechanism. We generated mCXCR2^–/–, mCXCR2^+/–, and wild-type nude mice following crosses between BALB/c mice heterozygous for nude^+/– and heterozygous for mCXCR2^+/–. We observed a significant inhibition of human melanoma tumor growth and experimental lung metastasis in mCXCR2^–/– mice as compared with wild-type nude mice. Inhibition in tumor growth and metastasis was associated with a decrease in melanoma cell proliferation, survival, inflammatory response, and angiogenesis. Together, these studies show the importance of host CXCR2–dependent CXCL-8–mediated angiogenesis in the regulation of melanoma growth and metastasis. [Cancer Res 2009;69(2):411–5]

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