alexa Paradoxical Augmentation of Tumor Angiogenesis Combined with Down-Regulation of IP-10 after Adenovirus-Mediated Transfer of Vasohibin-1 Gene in Cancer Cells
ISSN: 1948-5956

Journal of Cancer Science & Therapy
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Review Article

Paradoxical Augmentation of Tumor Angiogenesis Combined with Down-Regulation of IP-10 after Adenovirus-Mediated Transfer of Vasohibin-1 Gene in Cancer Cells

Takanobu Nakamura1,2, Yasuhiro Suzuki1, Yoshifumi Takahashi1, Susumu Satomi2 and Yasufumi Sato1*
1Department of Vascular Biology, Institute of Development, Aging and Cancer, Tohoku University, 4-1, Seiryo-machi, Aoba-ku, Sendai, Japan
2Department of Advanced Surgical Science and Technology, Tohoku University School of Medicine, 2-1, Seiryo-machi, Aoba-ku, Sendai, Japan
Corresponding Author : Yasufumi Sato
Department of Vascular Biology
Institute of Development
Aging and Cancer, Tohoku University, 4-1
Seiryo-machi, Aoba-ku
Sendai 980-8575, Japan
Tel: +81-22-717-8528
Fax: +81-22-717-8533
E-mail: [email protected]
Received June 20, 2014; Accepted August 08, 2014; Published August 11, 2014
Citation: Nakamura T, Suzuki Y, Takahashi Y, Satomi S, Sato Y (2014) Paradoxical Augmentation of Tumor Angiogenesis Combined with Down-Regulation of IP-10 after Adenovirus-Mediated Transfer of Vasohibin-1 Gene in Cancer Cells. J Cancer Sci Ther 6:289-297. doi:10.4172/1948-5956.1000283
Copyright: © 2014 Nakamura T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Vasohibin-1 (VASH1) is an endogenous angiogenesis inhibitor produced by the endothelium. Here we examined the efficacy of local adenovirus-mediated VASH1 gene transfer for anti-angiogenic cancer treatment. When non-proliferative adenovirus vector encoding the human VASH1 gene (AdhVASH1) was injected locally into the peritoneal cavity and HM-1 ovarian cancer cells were inoculated into the peritoneal cavity thereafter, we observed a significant inhibition of tumor angiogenesis. However, to our surprise, when HM-1 cells were infected with AdhVASH1 (HM-1/hVASH1) and then inoculated in mice, we observed a paradoxical augmentation of tumor angiogenesis and tumor growth. To explore the mechanism of this augmented tumor angiogenesis, we investigated the expression of various angiogenesis regulators. The level of angiogenesis stimulators such as VEGF and FGF-2 was unchanged; however we noticed a marked down-regulation of one angiogenesis inhibitor, namely interferon- γ-inducible protein-10 (IP-10). Moreover, this down-regulation of IP-10 and augmented tumor angiogenesis were not seen when HM-1/hVASH1 cells were inoculated into severe combined immunodeficiency mice. Our present analysis reveals that there is a mutual interaction between 2 angiogenesis inhibitors; VASH1 and IP-10, and the immune reaction might be responsible for this interaction through hitherto unknown mechanism. It also discloses the importance of endogenous IP-10 in tumors, as down-regulation of IP-10 results in the paradoxical augmentation of tumor angiogenesis. Care must be taken when VASH1 gene is transiently transferred to cancer cells for the antiangiogenesis treatment.

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