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タイトル: | UCHL1 provides diagnostic and antimetastatic strategies due to its deubiquitinating effect on HIF-1α |
著者: | Goto, Yoko Zeng, Lihua Yeom, Chan Joo Zhu, Yuxi Morinibu, Akiyo Shinomiya, Kazumi Kobayashi, Minoru https://orcid.org/0000-0003-3843-3584 (unconfirmed) Hirota, Kiichi Itasaka, Satoshi Yoshimura, Michio https://orcid.org/0000-0001-6665-2245 (unconfirmed) Tanimoto, Keiji Torii, Masae Sowa, Terumasa Menju, Toshi Sonobe, Makoto Kakeya, Hideaki https://orcid.org/0000-0002-4293-7331 (unconfirmed) Toi, Masakazu https://orcid.org/0000-0003-1488-9958 (unconfirmed) Date, Hiroshi Hammond, Ester M. Hiraoka, Masahiro Harada, Hiroshi https://orcid.org/0000-0001-7507-3173 (unconfirmed) |
著者名の別形: | 森鳰, 章代 小林, 稔 吉村, 通央 原田, 浩 鳥井, 雅恵 掛谷, 秀昭 戸井, 雅和 伊達, 洋至 園部, 誠 |
キーワード: | Biological sciences Cancer |
発行日: | 23-Jan-2015 |
出版者: | Nature Publishing Group |
誌名: | Nature communications |
巻: | 6 |
論文番号: | 6153 |
抄録: | Hypoxia-inducible factor 1 (HIF-1) plays a role in tumour metastases; however, the genes that activate HIF-1 and subsequently promote metastases have yet to be identified. Here we show that Ubiquitin C-terminal hydrolase-L1 (UCHL1) abrogates the von Hippel–Lindau-mediated ubiquitination of HIF-1α, the regulatory subunit of HIF-1, and consequently promotes metastasis. The aberrant overexpression of UCHL1 facilitates distant tumour metastases in a HIF-1-dependent manner in murine models of pulmonary metastasis. Meanwhile, blockade of the UCHL1–HIF-1 axis suppresses the formation of metastatic tumours. The expression levels of UCHL1 correlate with those of HIF-1α and are strongly associated with the poor prognosis of breast and lung cancer patients. These results indicate that UCHL1 promotes metastases as a deubiquitinating enzyme for HIF-1α, which justifies exploiting it as a prognostic marker and therapeutic target of cancers. |
著作権等: | This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. |
URI: | http://hdl.handle.net/2433/216128 |
DOI(出版社版): | 10.1038/ncomms7153 |
PubMed ID: | 25615526 |
出現コレクション: | 学術雑誌掲載論文等 |
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