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Stabilization of P/CAF, as a ubiquitin ligase toward MDM2, suppresses mitotic cell death through p53-p21 activation in HCT116 cells with SIRT2 suppression
https://repository.lib.tottori-u.ac.jp/records/7107
https://repository.lib.tottori-u.ac.jp/records/7107d5192079-84b0-4512-b6fe-4089fe976b73
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
bbrc508(1)_230.pdf (1.8 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2018-12-26 | |||||
| タイトル | ||||||
| タイトル | Stabilization of P/CAF, as a ubiquitin ligase toward MDM2, suppresses mitotic cell death through p53-p21 activation in HCT116 cells with SIRT2 suppression | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 主題 | SIRT2 | |||||
| キーワード | ||||||
| 主題 | P/CAF | |||||
| キーワード | ||||||
| 主題 | MDM2 | |||||
| キーワード | ||||||
| 主題 | p53 | |||||
| キーワード | ||||||
| 主題 | p21 | |||||
| キーワード | ||||||
| 主題 | mitotic cell death. | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題 | SIRT2 | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題 | P/CAF | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題 | MDM2 | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題 | p53 | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題 | p21 | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題 | mitotic cell death. | |||||
| 資源タイプ | ||||||
| 資源タイプ | journal article | |||||
| 著者 |
リ, イエンズ
× リ, イエンズ× コクラ, ケンジ× イノウエ, トシアキ× Li, Yanze |
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| 著者所属 | ||||||
| 値 | Division of Human Genome Science, School of Life Sciences, Faculty of Medicine, Tottori University / Department of Biochemistry and Molecular Biology, Harbin Medical University | |||||
| 著者所属 | ||||||
| 値 | Division of Human Genome Science, School of Life Sciences, Faculty of Medicine, Tottori University | |||||
| 著者所属 | ||||||
| 値 | Division of Human Genome Science, School of Life Sciences, Faculty of Medicine, Tottori University | |||||
| 著者所属（英） | ||||||
| 言語 | en | |||||
| 値 | Division of Human Genome Science, School of Life Sciences, Faculty of Medicine, Tottori University / Department of Biochemistry and Molecular Biology, Harbin Medical University | |||||
| 著者所属（英） | ||||||
| 言語 | en | |||||
| 値 | Division of Human Genome Science, School of Life Sciences, Faculty of Medicine, Tottori University | |||||
| 著者所属（英） | ||||||
| 言語 | en | |||||
| 値 | Division of Human Genome Science, School of Life Sciences, Faculty of Medicine, Tottori University | |||||
| 抄録 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | We previously reported that the suppression of SIRT2, an NAD + -dependent protein deacetylases, induces p53 accumulation via degradation of p300 and the subsequent MDM2 degradation, eventually leading to apoptosis in HeLa cells. The present study identified a novel pathway of p53 accumulation by SIRT2 suppression in HCT116(p53+/+) cells in which SIRT2 suppression led to escape from mitotic cell death caused by spindle assembly checkpoint activation induced by microtubule inhibitors such as nocodazole but not apoptosis or G1 or G2 arrest. We found that SIRT2 interacts with P/CAF, a histone acetyltransferase, which also acts as a ubiquitin ligase against MDM2. SIRT2 suppression led to an increase of P/CAF acetylation and its stabilization followed by a decrease in MDM2 and activation of the p53-p21 pathway. Depression of mitotic cell death in HCT116(p53+/+) cells with SIRT2 suppression was released by suppression of P/CAF or p21. Thus, the P/CAF-MDM2-p53-p21 axis enables the escape from mitotic cell death and confers resistance to nocodazole in HCT116(p53+/+) cells with SIRT2 suppression. As SIRT2 has attracted attention as a potential target for cancer therapeutics for p53 regulation, the present study provides a molecular basis for the efficacy of SIRT2 for future cancer therapy based on p53 regulation. These findings also suggest an undesirable function of the SIRT2 suppression associated with activation of the p53-p21 pathway in the suppression of mitotic cell death caused by spindle assembly checkpoint activation. | |||||
| 書誌情報 |
Biochemical and biophysical research communications en : Biochemical and biophysical research communications 巻 508, 号 1, p. 230-236, 発行日 2019-01-01 |
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| 出版者 | ||||||
| 出版者 | Elsevier Inc. | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0006291X | |||||
| 書誌レコードID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA11542044 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1016/j.bbrc.2018.11.136 | |||||
| 権利 | ||||||
| 権利情報 | Copyright © 2018 Elsevier Inc. All rights reserved. This manuscript version is made available under the CC-BY-NC-ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/ | |||||
| 情報源 | ||||||
| 関連名称 | This work was published by Elsevier : Li, Yanze, Kenji Kokura, and Toshiaki Inoue. "Stabilization of P/CAF, as a ubiquitin ligase toward MDM2, suppresses mitotic cell death through p53-p21 activation in HCT116 cells with SIRT2 suppression." Biochemical an | |||||
| 関連サイト | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | https://www.sciencedirect.com/science/article/pii/S0006291X18325683 | |||||
| 関連名称 | https://www.sciencedirect.com/science/article/pii/S0006291X18325683 | |||||
| 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 | |||||
