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Adrenomedullin antagonist suppresses tumor formation in renal cell carcinoma through inhibitory effects on tumor endothelial cells and endothelial progenitor mobilization.

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Title: Adrenomedullin antagonist suppresses tumor formation in renal cell carcinoma through inhibitory effects on tumor endothelial cells and endothelial progenitor mobilization.
Authors: Tsuchiya, Kunihiko Browse this author
Hida, Kyoko Browse this author
Hida, Yasuhiro Browse this author
Muraki, Chikara Browse this author
Ohga, Noritaka Browse this author
Akino, Tomoshige Browse this author
Kondo, Takeshi Browse this author
Miseki, Tetsuya Browse this author
Nakagawa, Koji Browse this author
Shindoh, Masanobu Browse this author
Harabayashi, Toru Browse this author
Shinohara, Nobuo Browse this author
Nonomura, Katsuya Browse this author
Kobayashi, Masanobu Browse this author
Issue Date: Jun-2010
Journal Title: International journal of oncology
Volume: 36
Issue: 6
Start Page: 1379
End Page: 1386
PMID: 20428760
Abstract: Adrenomedullin (AM) is a multifunctional 52-amino acid peptide. AM has several effects and acts as a growth factor in several types of cancer cells. Our previous study revealed that an AM antagonist (AMA) suppressed the growth of pancreatic tumors in mice, although its mechanism was not elucidated. In this study, we constructed an AMA expression vector and used it to treat renal cell carcinoma (RCC) in mice. This AMA expression vector significantly reduced tumor growth in mice. In addition, microvessel density was decreased in AMA-treated tumors. To analyze the effect of AMA on tumor angiogenesis in this model, tumor endothelial cells (TECs) were isolated from RCC xenografts. TEC proliferation was stimulated by AM and it was inhibited by AMA significantly. AM induced migration of TECs and it was also blocked by AMA. However, normal ECs (NECs) were not affected by either AM or AMA. These results demonstrate that AMA has inhibitory effects on TECs specifically, not on NEC, thereby inhibiting tumor angiogenesis. Furthermore, we showed that vascular endothelial growth factor-induced mobilization of endothelial progenitor cell (EPC) into circulation was inhibited by AMA. These results suggest that AMA can be considered a good anti-angiogenic reagent that selectively targets TECs and EPC in renal cancer.
Type: article
URI: http://hdl.handle.net/2115/47207
Appears in Collections:歯学院・歯学研究院 (Graduate School of Dental Medicine / Faculty of Dental Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 樋田 京子

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