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Research Articles: Therapeutics

Inhibition of human nasopharyngeal carcinoma growth and metastasis in mice by adenovirus-associated virus–mediated expression of human endostatin

Departments of ¹ Otolaryngology and ² Gastroenterology, Nanfang Hospital, Nanfang Medical University; ³ Department of Neurology, The Second Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China; ⁴ Department of Chemistry, Open Laboratory of Chemical Biology of the Institute of Molecular Technology for Drug Discovery, The University of Hong Kong; and ⁵ Li Ka Shing Institute of Health Sciences and Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Hong Kong, China

Requests for reprints: Marie C. Lin, Department of Chemistry, 8/F Kadoorie Biological Science Building, The University of Hong Kong, Pokfulam, Hong Kong, China. Phone: 852-2299-0776; Fax: 852-2817-1006. E-mail: mcllin{at}hkusua.hku.hk

Nasopharyngeal carcinoma (NPC) is a highly malignant and frequently metastasized tumor. Endostatin has been shown to inhibit NPC growth, but its efficacy against NPC metastasis has not been shown in vivo. Here, we established a NPC metastasis model in mice by transplanting EBV-positive NPC cells, C666-1, in the livers of nude mice and observed lung metastasis. Furthermore, we showed that tail vein injection of recombinant adeno-associated virus encoding human endostatin (rAAV-hEndo) significantly prolonged the median survival rate of NPC metastasis–bearing mice (from 22 to 37 days, P < 0.01). The rAAV-hEndo treatment resulted in a statistically significant reduction in tumor growth and microvessel formation. It also increased the apoptotic index in the primary liver tumor but not in the normal liver tissue. Importantly, no formation of liver or lung metastasis was detected. The potent inhibition of NPC metastasis suggests the feasibility of combining rAAV-hEndo gene therapy with other therapies for the prevention and treatment of NPC metastasis. [Mol Cancer Ther 2006;5(5):1290–8]

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Received 8/30/05; revised 1/25/06; accepted 3/ 2/06.

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