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p53 mutation in colon cancer.
https://doi.org/10.24517/00053861
https://doi.org/10.24517/00053861ddaf17da-f857-4d15-8f81-656465cca003
| 名前 / ファイル | ライセンス | アクション |
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FR-PR-OSHIMA-M-mjy075.pdf (879.6 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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| 公開日 | 2019-04-12 | |||||||||
| タイトル | ||||||||||
| タイトル | p53 mutation in colon cancer. | |||||||||
| 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 | 10.24517/00053861 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Nakayama, Mizuho
× Nakayama, Mizuho× Oshima, Masanobu |
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| 著者別表示 |
中山, 瑞穂
× 中山, 瑞穂
× 大島, 正伸
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| 提供者所属 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 金沢大学ナノ生命科学研究所 | |||||||||
| 書誌情報 |
Journal of Molecular Cell Biology p. mjy075, 発行日 2018-11-29 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 1674-2788 | |||||||||
| DOI | ||||||||||
| 関連タイプ | isIdenticalTo | |||||||||
| 識別子タイプ | DOI | |||||||||
| 関連識別子 | 10.1093/jmcb/mjy075 | |||||||||
| 出版者 | ||||||||||
| 出版者 | Chinese Academy of Sciences / Oxford University Press | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | The accumulation of genetic alterations in driver genes is responsible for the development and malignant progression of colorectal cancer. Comprehensive genome analyses have revealed the driver genes, including APC, KRAS, TGFBR2, and TP53, whose mutations are frequently found in human colorectal cancers. Among them, the p53 mutation is found in ~60% of colorectal cancers, and a majority of mutations are missense-type at ‘hot spots’, suggesting an oncogenic role of mutant p53 by ‘gain-of-function’ mechanisms. Mouse model studies have shown that one of these missense-type mutations, p53 R270H (corresponding to human R273H), causes submucosal invasion of intestinal tumors, while the loss of wild-type p53 has a limited effect on the invasion process. Furthermore, the same mutant p53 promotes metastasis when combined with Kras activation and TGF-β suppression. Importantly, either missense-type p53 mutation or loss of wild-type p53 induces NF-κB activation by a variety of mechanisms, such as increasing promoter accessibility by chromatin remodeling, which may contribute to progression to epithelial–mesenchymal transition. These results indicate that missense-type p53 mutations together with loss of wild-type p53 accelerate the late stage of colorectal cancer progression through the activation of both oncogenic and inflammatory pathways. Accordingly, the suppression of the mutant p53 function via the inhibition of nuclear accumulation is expected to be an effective strategy against malignant progression of colorectal cancer. | |||||||||
| 権利 | ||||||||||
| 権利情報 | Copyright © Chinese Academy of Sciences / Oxford University Press | |||||||||
| 著者版フラグ | ||||||||||
| 出版タイプ | VoR | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||
| 関連URI | ||||||||||
| 識別子タイプ | URI | |||||||||
| 関連識別子 | https://academic.oup.com/jmcb/advance-article/doi/10.1093/jmcb/mjy075/5212692 | |||||||||
| 関連名称 | https://academic.oup.com/jmcb/advance-article/doi/10.1093/jmcb/mjy075/5212692 | |||||||||
