Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/28603
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 18034/20233 (89%)
Visitors : 23631712      Online Users : 727
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/28603


    Title: Induction of Apurinic Endonuclease 1 Overexpression by Endoplasmic Reticulum Stress in Hepatoma Cells
    Authors: Cheng, Tsung-Lin
    Chen, Pin-Shern
    Li, Ren-Hao
    Yuan, Shyng-Shiou
    Su, Ih-Jen
    Hung, Jui-Hsiang
    Contributors: 生物科技系
    新藥創建研究中心
    Keywords: hepatocellular carcinoma
    Huh-7
    HepG2
    NeHepLxHT
    hepatitis B virus
    hepatitis B virus pre-S2 Delta large mutant surface protein
    endoplasmic reticulum stress
    apurinic endonuclease 1
    GRP78
    Date: 2014-07
    Issue Date: 2015-05-06 21:22:11 (UTC+8)
    Publisher: Mdpi Ag
    Abstract: Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide with poor prognosis due to resistance to conventional chemotherapy and limited efficacy of radiotherapy. Previous studies have noted the induction of endoplasmic reticulum stress or apurinic endonuclease 1 (APE1) expression in many tumors. Therefore, the aim of this study was to investigate the relationship between endoplasmic reticulum (ER stress) and APE1 in hepatocellular carcinoma. Here we investigate the expression of APE1 during ER stress in HepG2 and Huh-7 cell lines. Tunicamycin or brefeldin A, two ER stress inducers, increased APE1 and GRP78, an ER stress marker, expression in HepG2 and Huh-7 cells. Induction of APE1 expression was observed through transcription level in response to ER stress. APE1 nuclear localization during ER stress was determined using immunofluorescence assays in HepG2 cells. Furthermore, expression of Hepatitis B virus pre-S2 Delta large mutant surface protein (pre-S2 Delta), an ER stress-induced protein, also increased GRP78 and APE1 expression in the normal hepatocyte NeHepLxHT cell line. Similarly, tumor samples showed higher expression of APE1 in ER stress-correlated liver cancer tissue in vivo. Our results demonstrate that ER stress and HBV pre-S2 Delta increased APE1 expression, which may play an important role in resistance to chemotherapeutic agents or tumor development. Therefore, these data provide an important chemotherapeutic strategy in ER stress and HBV pre-S2 Delta-associated tumors.
    Relation: International Journal of Molecular Sciences, v.15 n.7, pp.12442-12457
    Appears in Collections:[Dept. of Biotechnology (including master's program)] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML1346View/Open


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


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback