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Hepatocyte growth factor and Met in tumor biology and therapeutic approach with NK4
https://doi.org/10.24517/00027398
https://doi.org/10.24517/00027398324c539c-22cd-4b0c-8203-28a859fce23a
| 名前 / ファイル | ライセンス | アクション |
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CA-PR-MATSUMOTO-K-3360.pdf (6.0 MB)
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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 | Hepatocyte growth factor and Met in tumor biology and therapeutic approach with NK4 | |||||||||||
| 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 | 10.24517/00027398 | |||||||||||
| ID登録タイプ | JaLC | |||||||||||
| 著者 |
松本, 邦夫
× 松本, 邦夫× Nakamura, Takahiro× Sakai, Katsuya× Nakamura, Toshikazu |
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| 著者別表示 |
松本, 邦夫
× 松本, 邦夫
× 中村, 隆弘
× 酒井, 克也
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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分子標的がん医療研究開発センター | |||||||||||
| 書誌情報 |
Proteomics 巻 8, 号 16, p. 3360-3370, 発行日 2008-08-01 |
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| ISSN | ||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||
| 収録物識別子 | 1615-9853 | |||||||||||
| NCID | ||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||
| 収録物識別子 | AA11556661 | |||||||||||
| DOI | ||||||||||||
| 関連タイプ | isVersionOf | |||||||||||
| 識別子タイプ | DOI | |||||||||||
| 関連識別子 | 10.1002/pmic.200800156 | |||||||||||
| 出版者 | ||||||||||||
| 出版者 | Karger | |||||||||||
| 抄録 | ||||||||||||
| 内容記述タイプ | Abstract | |||||||||||
| 内容記述 | Hepatocyte growth factor (HGF) and Met/HGF receptor tyrosine kinase play a role in the progression to invasive and metastatic cancers. A variety of cancer cells secrete molecules that enhance HGF expression in stromal fibroblasts, while fibroblast-derived HGF, in turn, is a potent stimulator of the invasion of cancer cells. In addition to the ligand-dependent activation, Met receptor activation is negatively regulated by cell-cell contact and Ser985 phosphorylation in the juxtamembrane of Met. The loss of intercellular junctions may facilitate an escape from the cell-cell contact-dependent suppression of Met-signaling. Significance of juxtamembrane mutations found in human cancers is assumed to be a loss-of-function in the negative regulation of Met. In attempts to block the malignant behavior of cancers, NK4 was isolated as a competitive antagonist against HGF-Met signaling. Independently on its HGF-antagonist action, NK4 inhibited angiogenesis induced by vascular endothelial cell growth factor and basic fibroblast growth factor, as well as HGF. In experimental models of distinct types of cancers, NK4 inhibited Met activation and this was associated with inhibition of tumor invasion and metastasis. NK4 inhibited tumor angiogenesis, thereby suppressing angiogenesis-dependent tumor growth. Cancer treatment with NK4 suppresses malignant tumors to be "static" in both tumor growth and spreading. © 2008 Wiley-VCH Verlag GmbH & Co. KGaA. | |||||||||||
| 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 | |||||||||||
