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Norepinephrine Up-regulates the Expression of Vascular Endothelial Growth Factor, Matrix Metalloproteinase (MMP)-2, and MMP-9 in Nasopharyngeal Carcinoma Tumor Cells

¹ Department of Molecular Virology, Immunology, and Medical Genetics, ² Institute for Behavioral Medicine Research, ³ Comprehensive Cancer Center, ⁴ The Dorothy M. Davis Heart and Lung Research Institute, Departments of ⁵ Pathology and ⁶ Internal Medicine, The Ohio State University Medical Center; ⁷ School of Public Health and ⁸ The Center for Biostatistics, The Ohio Sate University, Columbus, Ohio; and ⁹ Departments of Gynecologic Oncology and Cancer Biology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas

Requests for reprints: Ronald Glaser, Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, 333 West 10th Avenue, 2175 Graves Hall, Columbus, OH 43210. Phone: 614-292-5526; Fax: 614-292-1011; E-mail: ronald.glaser{at}osumc.edu.

Recent studies using ovarian cancer cells have shown that the catecholamine hormones norepinephrine (norepi) and epinephrine (epi) may influence cancer progression by modulating the expression of matrix metalloproteinases (MMP) and vascular endothelial growth factor (VEGF). The purpose of this study is to determine if the stress hormone norepi can influence the expression of MMP-2, MMP-9, and VEGF in nasopharyngeal carcinoma (NPC) tumors by using three NPC tumor cell lines. The NPC cell lines HONE-1, HNE-1, and CNE-1 were treated with norepi. The effects of norepi on MMP-2, MMP-9, and VEGF synthesis were measured by ELISA; functional MMP activity was measured by the invasive potential of the cells using a membrane invasion culture system whereas functional activity of VEGF was analyzed using a human umbilical vein endothelial cell tube formation assay. Norepi treatment increased MMP-2, MMP-9, and VEGF levels in culture supernatants of HONE-1 cells, which could be inhibited by the ß-blocker propranolol. Norepi induced the invasiveness of all NPC cell lines in a dose-dependent manner, which was blocked by CMT-3, an MMP inhibitor, and propranolol. Norepi stimulated the release of functional angiogenic VEGF by HONE-1 cells as well. Finally, HONE-1 cells were shown to express ß-adrenergic receptors as did seven of seven NPC biopsies examined. The data suggest that catecholamine hormones produced by the sympathetic-adrenal medullary axis may affect NPC tumor progression, in part, through modulation of key angiogenic cytokines. (Cancer Res 2006; 66(21): 10357-64)

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