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A Glycolytic Mechanism Regulating an Angiogenic Switch in Prostate Cancer

¹ Department of Periodontics and Oral Medicine, ² Department of Cariology, Restorative Sciences, and Endodontics, and ³ Division of Prosthodontics, Department of Biologic and Materials Sciences, University of Michigan School of Dentistry; ⁴ Department of Urology and ⁵ Division of Internal Medicine and Urology, University of Michigan School of Medicine, Ann Arbor, Michigan and ⁶ Center for Vascular Research, University of New South Wales, Sydney, New South Wales, Australia

Requests for reprints: Russell S. Taichman, Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, 1011 North University Avenue, Ann Arbor, MI 48109-1078. Phone: 734-764-9952; Fax: 734-763-5503; E-mail: rtaich{at}umich.edu.

The generation of an ‘angiogenic switch’ is essential for tumor growth, yet its regulation is poorly understood. In this investigation, we explored the linkage between metastasis and angiogenesis through CXCL12/CXCR4 signaling. We found that CXCR4 regulates the expression and secretion of the glycolytic enzyme phosphoglycerate kinase 1 (PGK1). Overexpression of PGK1 reduced the secretion of vascular endothelial growth factor and interleukin-8 and increased the generation of angiostatin. At metastatic sites, however, high levels of CXCL12 signaling through CXCR4 reduced PGK1 expression, releasing the angiogenic response for metastastic growth. These data suggest that PGK1 is a critical downstream target of the chemokine axis and an important regulator of an ‘angiogenic switch’ that is essential for tumor and metastatic growth. [Cancer Res 2007;67(1):149–59]

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