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

Tsuchiya, Kunihiko; Hida, Kyoko; Hida, Yasuhiro et al.

International journal of oncology, 2010, 36(6), 1379-1386

Permalink : https://hdl.handle.net/2115/47207

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アクセス権
open access
URI
https://hdl.handle.net/2115/47207
タイトル
Adrenomedullin antagonist suppresses tumor formation in renal cell carcinoma through inhibitory effects on tumor endothelial cells and endothelial progenitor mobilization.
著者
Tsuchiya, Kunihiko ; Hida, Kyoko ; Hida, Yasuhiro ; Muraki, Chikara ; Ohga, Noritaka ; Akino, Tomoshige ; Kondo, Takeshi ; Miseki, Tetsuya ; Nakagawa, Koji ; Shindoh, Masanobu ; Harabayashi, Toru ; Shinohara, Nobuo ; Nonomura, Katsuya ; Kobayashi, Masanobu
著者名
Tsuchiya, Kunihiko
著者名
Hida, Kyoko
著者名
Hida, Yasuhiro
著者名
Muraki, Chikara
著者名
Ohga, Noritaka
著者名
Akino, Tomoshige
著者名
Kondo, Takeshi
著者名
Miseki, Tetsuya
著者名
Nakagawa, Koji
著者名
Shindoh, Masanobu
著者名
Harabayashi, Toru
著者名
Shinohara, Nobuo
著者名
Nonomura, Katsuya
著者名
Kobayashi, Masanobu
言語
英語
発行日
2010-06
収録物名
International journal of oncology
巻(号)
36(6)
ページ
1379-1386
抄録
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.
資源タイプ
学術雑誌論文
出版タイプ
Version of Record
PISSN
1791-2423
EISSN
1791-2423
関連情報
PMID
20428760
関連情報 (isIdenticalTo)
出版社版DOI
https://doi.org/10.3892/ijo_00000622