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Breast Cancer Growth Is Inhibited by Vasoactive Intestinal Peptide (VIP) Hybrid, a Synthetic VIP Receptor Antagonist

Biomarkers and Prevention Research Branch, National Cancer Institute, Rockville, Maryland 20850 [H. Z., T. H., S. J., M. B., T. W. M.]; Israel Institute for Biological Research, Ness-Ziona, Israel [Y. G.]; Division of Cell Biology and Experimental Cancer Research, Institute of Pathology, University of Berne, Berne, Switzerland [J. C. R.]; Department of Organic Chemistry, Weizmann Institute of Science, Rehovot [M. F.]; and Department of Chemical Pathology, Sackler School of Medicine, Tel Aviv [I. G.], Israel

Breast cancer vasoactive intestinal peptide (VIP) receptors were characterized. Using in vitro autoradiographic techniques, ¹²⁵I-labeled VIP bound with high affinity to breast biopsy sections. ¹²⁵I-labeled VIP bound specifically to five breast cancer cell lines examined using receptor-binding techniques. Specific ¹²⁵I-labeled VIP binding to MDA-MB-231 cells was inhibited with high affinity by VIP and pituitary adenylate cyclase-activating polypeptide (IC^b50 = 2 nM) and with moderate affinity by the VIP hybrid (IC₅₀ = 0.5 µM) VIP elevated the cAMP in a dose-dependent manner, and VIP hybrid (10 µM) inhibited the increase in cAMP caused by VIP. Using Northern blot analysis, VIP (10 nM) stimulated c-fos and c-myc mRNA, and the increase caused by VIP was reversed by the VIP hybrid. The VIP hybrid inhibited breast cancer growth in vitro and in vivo using nude mice bearing breast cancer xenografts. These data suggest that the VIP hybrid is a breast cancer VIP receptor antagonist.

¹ To whom requests for reprints should be addressed, at National Cancer Institute, Biomarkers and Prevention Research Branch, 9610 Medical Center Drive, Building C, Room 300, Rockville, MD 20850. Phone: (301) 402-3128; Fax: (301) 402-4422.

Received 4/ 8/96. Accepted 5/31/96.

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