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Dysregulated HAI-2 Plays an Important Role in Renal Cell Carcinoma Bone Metastasis through Ligand-Dependent MET Phosphorylation
http://hdl.handle.net/10458/0002000105
http://hdl.handle.net/10458/00020001057d6ba7ae-bca6-4b46-bd0c-c75226f351e7
名前 / ファイル | ライセンス | アクション |
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Item type | 学術雑誌論文 / Journal Article(1) | |||||||||||
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公開日 | 2023-10-24 | |||||||||||
タイトル | ||||||||||||
タイトル | Dysregulated HAI-2 Plays an Important Role in Renal Cell Carcinoma Bone Metastasis through Ligand-Dependent MET Phosphorylation | |||||||||||
言語 | en | |||||||||||
言語 | ||||||||||||
言語 | eng | |||||||||||
キーワード | ||||||||||||
言語 | en | |||||||||||
主題Scheme | Other | |||||||||||
キーワード | RCC | |||||||||||
キーワード | ||||||||||||
言語 | en | |||||||||||
主題Scheme | Other | |||||||||||
キーワード | bone metastasis | |||||||||||
キーワード | ||||||||||||
言語 | en | |||||||||||
主題Scheme | Other | |||||||||||
キーワード | HGF | |||||||||||
キーワード | ||||||||||||
言語 | en | |||||||||||
主題Scheme | Other | |||||||||||
キーワード | MET | |||||||||||
キーワード | ||||||||||||
言語 | en | |||||||||||
主題Scheme | Other | |||||||||||
キーワード | HAI-2 | |||||||||||
資源タイプ | ||||||||||||
資源タイプ | journal article | |||||||||||
著者 |
山崎, 浩司
× 山崎, 浩司× 向井, 尚一郎× 杉江, 悟× 永井, 崇敬× 中原, 梢× 上別府, 豊治× Sakamoto, Hiromasa
× Shibasaki, Noboru
× Terada, Naoki× Toda, Yoshinobu
× 片岡, 寛章× 賀本, 敏行 |
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抄録 | ||||||||||||
内容記述タイプ | Abstract | |||||||||||
内容記述 | MET, a c-met proto-oncogene product and hepatocyte growth factor (HGF) receptor, is known to play an important role in cancer progression, including bone metastasis. In a previous study, we reported increased expression of MET and matriptase, a novel activator of HGF, in bone metastasis. In this study, we employed a mouse model of renal cell carcinoma (RCC) bone metastasis to clarify the significance of the HGF/MET signaling axis and the regulator of HGF activator inhibitor type-2 (HAI-2). Luciferase-transfected 786-O cells were injected into the left cardiac ventricle of mice to prepare the mouse model of bone metastasis. The formation of bone metastasis was confirmed by whole-body bioluminescent imaging, and specimens were extracted. Expression of HGF/MET-related molecules was analyzed. Based on the results, we produced HAI-2 stable knockdown 786-O cells, and analyzed invasiveness and motility. Expression of HGF and matriptase was increased in bone metastasis compared with the control, while that of HAI-2 was decreased. Furthermore, we confirmed increased phosphorylation of MET in bone metastasis. The expression of matriptase was upregulated, and both invasiveness and motility were increased significantly by knockdown of HAI-2. The significance of ligand-dependent MET activation in RCC bone metastasis is considered, and HAI-2 may be an important regulator in this system. | |||||||||||
言語 | en | |||||||||||
内容記述 | ||||||||||||
内容記述タイプ | Other | |||||||||||
内容記述 | Yamasaki, K.; Mukai, S.; Sugie, S.; Nagai, T.; Nakahara, K.; Kamibeppu, T.; Sakamoto, H.; Shibasaki, N.; Terada, N.; Toda, Y.; et al. Dysregulated HAI-2 Plays an Important Role in Renal Cell Carcinoma Bone Metastasis through Ligand-Dependent MET Phosphorylation. Cancers 2018, 10, 190. https://doi.org/10.3390/cancers10060190 | |||||||||||
言語 | en | |||||||||||
書誌情報 |
en : Cancers 巻 10, 号 6, p. 190, 発行日 2018-06-08 |
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出版者 | ||||||||||||
出版者 | MDPI | |||||||||||
言語 | en | |||||||||||
DOI | ||||||||||||
関連タイプ | isVersionOf | |||||||||||
識別子タイプ | DOI | |||||||||||
関連識別子 | https://doi.org/10.3390/cancers10060190 | |||||||||||
権利 | ||||||||||||
言語 | en | |||||||||||
権利情報 | © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). | |||||||||||
著者版フラグ | ||||||||||||
出版タイプ | VoR |
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Cite as
山崎, 浩司, 向井, 尚一郎, 杉江, 悟, 永井, 崇敬, 中原, 梢, 上別府, 豊治, Sakamoto, Hiromasa, Shibasaki, Noboru, Terada, Naoki, Toda, Yoshinobu, 片岡, 寛章, 賀本, 敏行, 2018, Dysregulated HAI-2 Plays an Important Role in Renal Cell Carcinoma Bone Metastasis through Ligand-Dependent MET Phosphorylation: MDPI, 190– p.
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