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J. Biol. Chem., Vol. 283, Issue 7, 4283-4294, February 15, 2008

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The Role of CXCR7/RDC1 as a Chemokine Receptor for CXCL12/SDF-1 in Prostate Cancer^*

Jianhua Wang, Yusuke Shiozawa, Jincheng Wang, Yu Wang, Younghun Jung, Kenneth J. Pienta, Rohit Mehra^¶, Robert Loberg, and Russell S. Taichman¹

From the Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, the Department of Internal Medicine, Division of Hematology/Oncology, and the ^¶Department of Pathology, University of Michigan School of Medicine, Ann Arbor, Michigan 48109

Several reports have recently documented that CXCR7/RDC1 functions as a chemokine receptor for SDF-1/CXCL12, which regulates a spectrum of normal and pathological processes. In this study, the role of CXCR7/RDC1 in prostate cancer (PCa) was explored. Staining of high density tissue microarrays demonstrates that the levels of CXCR7/RDC1 expression increase as the tumors become more aggressive. In vitro and in vivo studies with PCa cell lines suggest that alterations in CXCR7/RDC1 expression are associated with enhanced adhesive and invasive activities in addition to a survival advantage. In addition, it was observed that CXCR7/RDC1 levels are regulated by CXCR4. Among the potential downstream targets of CXCR7/RDC1 are CD44 and cadherin-11, which are likely to contribute to the invasiveness of PCa cells. CXCR7/RDC1 also regulates the expression of the proangiogenic factors interleukin-8 or vascular endothelial growth factor, which are likely to participate in the regulation of tumor angiogenesis. Finally, we found that signaling by CXCR7/RDC1 activates AKT pathways. Together, these data demonstrate a role for CXCR7/RDC1 in PCa metastasis and progression and suggest potential targets for therapeutic intervention.

Received for publication, September 6, 2007 , and in revised form, December 5, 2007.

^* This work was supported by National Institutes of Health NCI PO1 Awards CA93900 (to K. J. P. and R. S. T.) and DE13701 (to R. S. T.) and Department of Defense Grants DAMD 17-02-1-0100 and PC060857 (to R. S. T.) and supported by the National Institutes of Health through the University of Michigan's Cancer Support Center (Grant 5 P30 CA46592). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. 1-4.

¹ To whom correspondence should be addressed. Tel.: 734-764-9952; Fax: 734-763-5503; E-mail: rtaich{at}umich.edu.

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