English  |  正體中文  |  简体中文  |  Items with full text/Total items : 28611/40649
Visitors : 639142      Online Users : 43
RC Version 4.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Adv. Search
LoginUploadHelpAboutAdminister

Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/26851

Title: miR-122 targets an anti-apoptotic gene, Bcl-w, in human hepatocellular carcinoma cell lines
Authors: Cliff Ji-Fan Lin;Hong-Yi Gong;Hung-Chia Tseng;Wei-Lun Wang;Jen-Leih Wu
Contributors: NTOU:Department of Aquaculture
國立臺灣海洋大學:水產養殖學系
Keywords: miR-122;Bcl-w;Hepatocellular carcinoma
Date: 2008-10-24
Issue Date: 2011-10-21T02:19:07Z
Publisher: Biochemical and Biophysical Research Communications
Abstract: Abstract:miR-122, a hepato-specific microRNA (miRNA), is frequently down-regulated in human hepatocellular carcinoma (HCC). In an effort to identify novel miR-122 targets, we performed an in silico analysis and detected a putative binding site in the 3′-untranslated region (3′-UTR) of Bcl-w, an anti-apoptotic Bcl-2 family member. In the HCC-derived cell lines, Hep3B and HepG2, we confirmed that miR-122 modulates Bcl-w expression by directly targeting binding site within the 3′-UTR. The cellular mRNA and protein levels of Bcl-w were repressed by elevated levels of miR-122, which subsequently led to reduction of cell viability and activation of caspase-3. Thus, Bcl-w is a direct target of miR-122 that functions as an endogenous apoptosis regulator in these HCC-derived cell lines.
Relation: 375(3), pp.315-320
URI: http://ntour.ntou.edu.tw/handle/987654321/26851
Appears in Collections:[水產養殖學系] 期刊論文

Files in This Item:

File Description SizeFormat
index.html0KbHTML269View/Open


All items in NTOUR are protected by copyright, with all rights reserved.

 


著作權政策宣告: 本網站之內容為國立臺灣海洋大學所收錄之機構典藏,無償提供學術研究與公眾教育等公益性使用,請合理使用本網站之內容,以尊重著作權人之權益。
網站維護: 海大圖資處 圖書系統組
DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback