※一部利用できない機能があります
Tip60 regulates MT1-MMP transcription and invasion of glioblastoma cells through NF-κB pathway
- フォーマット:
- 論文
- 責任表示:
- Takino, Takahisa ; Nakada, Mitsutoshi ; Li, Zichen ; Yoshimoto, Taisuke ; Domoto, Takahiro ; Sato, Hiroshi
- 言語:
- 英語
- 出版情報:
- Springer Verlag, 2016-01-01
- 著者名:
Takino, Takahisa Nakada, Mitsutoshi Li, Zichen Yoshimoto, Taisuke Domoto, Takahiro Sato, Hiroshi - 掲載情報:
- Clinical and Experimental Metastasis
- ISSN:
- 0262-0898
- 巻:
- 33
- 通号:
- 1
- 開始ページ:
- 45
- 終了ページ:
- 52
- バージョン:
- author
- 概要:
- A histone acetyltransferase Tat-interacting protein 60 kDa (Tip60) regulates the DNA damage response by acetylating histone and remodeling chromatin. In addition to histone acetyltransferase activity, Tip60 is known to regulate a variety of cellular functions, including gene expression, DNA damage response, cell migration and apoptosis. Lower expression of Tip60 is observed in lymphomas, melanomas, breast, colon, and lung cancer. It is widely accepted that Tip60 … functions as a tumor suppressor. However, a role of Tip60 in gliomas still remains unclear. In this study, we investigated the role of Tip60 in the malignant behavior of human gliomas. By quantitative RT-PCR analysis using fresh human brain tumor tissues from 55 patients, we found that lower Tip60 expression and higher membrane-type 1 matrix metalloproteinase (MT1-MMP) expression are associated with advanced tumor grade in glioma tissues. Knockdown of Tip60 in glioblastoma cells promoted cell adhesion, spreading and MT1-MMP transcription and thereby invasion, which was suppressed by inhibition of MT1-MMP and nuclear factor-kappa B (NF-κB) activity. We demonstrate for the first time that tumor suppressor Tip60 down-regulates cell adhesion and MT1-MMP expression and thereby invasion of glioblastoma cells by suppressing NF-κB pathway. © 2015 Springer Science+Business Media Dordrecht<br />Embargo Period 12 months 続きを見る
- URL:
- http://hdl.handle.net/2297/43905
類似資料:
Japanese Cancer Association = 日本癌学会 / John Wiley & Sons | |
Academic Press / Elsevier | |
金沢大学がん研究所 | |
金沢大学がん研究所 | |
Japanese Cancer Association / Blackwell Publishing Ltd |