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The β1-integrin-dependent function of RECK in physiologic and tumor angiogenesis
https://doi.org/10.24517/00027527
https://doi.org/10.24517/000275271e8279e5-337e-4007-b896-c9f504404c63
名前 / ファイル | ライセンス | アクション |
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CA-PR-TAKAHASHI-C-665.pdf (988.8 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-05 | |||||
タイトル | ||||||
タイトル | The β1-integrin-dependent function of RECK in physiologic and tumor angiogenesis | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
ID登録 | ||||||
ID登録 | 10.24517/00027527 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Miki, Takao
× Miki, Takao× Shamma, Awad× Kitajima, Shunsuke× Takegami, Yujiro× Noda, Makoto× Nakashima, Yasuaki× Watanabe, Kenichiro× Takahashi, Chiaki |
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著者別表示 |
三木, 貴雄
× 三木, 貴雄× 北嶋, 俊輔× 野田, 亮× 高橋, 智聡 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学がん研究所 | |||||
書誌情報 |
Molecular Cancer Research 巻 8, 号 5, p. 655-676, 発行日 2010-05-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1541-7786 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA11795083 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1158/1541-7786.MCR-09-0351 | |||||
出版者 | ||||||
出版者 | American Association for Cancer Research | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Vascular endothelial cells produce considerable amounts of matrix metalloproteinases (MMP), including MMP-2, MMP-9, and membrane type 1 (MT1)-MMP. However, little is known about the regulatory mechanisms of these protease activities exhibited during vascular development. A glycosylphosphatidylinositol-anchored glycoprotein, reversion-inducing cysteine-rich protein with Kazal motifs (RECK), has been shown to attenuate MMP-2 maturation by directly interacting with MT1-MMP. Here, we show that an angiogenic factor angiopoietin-1 induces RECK expression in human umbilical vein endothelial cells (HUVEC), and RECK depletion in these cells results in defective vascular tube formation and cellular senescence. We further observed that RECK depletion downregulates β1-integrin activation, which was associated with decreased autophosphorylation of focal adhesion kinase and increased expression of a cyclin-dependent kinase inhibitor p21CIP1. In agreement, significant downregulation of β1-integrin activity was observed in vascular endothelial cells in Reck-/- mouse embryos. In HUVECs, specific inhibition of MMP-2 significantly antagonized the effect of RECK depletion on β1-integrin signaling, cell proliferation, and tube elongation. Furthermore, we observed that hypervascular tumor-derived cell lines can induce high RECK expression in convoluted vascular endothelial cells, and this in turn supports tumor growth. Targeting RECK specifically in tumor-associated vascular endothelial cells resulted in tumor regression. Therefore, we propose that RECK in tumor vascular endothelial cells can be an interesting target of cancer treatment via abortion of tumor angiogenesis. ©2010 AACR. | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa |