國家衛生研究院 NHRI:Item 3990099045/9336
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 852184      Online Users : 1409
RC Version 6.0 © 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
    Home ‧ Login ‧ Upload ‧ Help ‧ About ‧ Administer Goto mobile version


    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/9336


    Title: Regulation of Aldo-keto-reductase family 1 B10 by 14-3-3epsilon and their prognostic impact of hepatocellular carcinoma
    Authors: Liu, TA;Jan, YJ;Ko, BS;Wu, YJ;Lu, YJ;Liang, SM;Liu, CC;Chen, SC;Wang, J;Shyue, SK;Liou, JY
    Contributors: Institute of Cellular and Systems Medicine
    Abstract: 14-3-3epsilon is overexpressed in hepatocellular carcinoma (HCC) and its expression significantly associates with a poor prognostic outcome. To uncover how 14-3-3epsilon contributes to the tumor progression of HCC, we investigated the potential downstream targets regulated by 14-3-3epsilon. We found that 14-3-3epsilon increases expression and nuclear translocation of beta-catenin and that 14-3-3epsilon-induced cell proliferation is attenuated by beta-catenin silencing in HCC cells. Moreover, 14-3-3epsilon induces aldo-keto reductase family 1 member B10 (AKR1B10) expression through the activation of beta-catenin signaling. Knockdown of AKR1B10 by siRNAs abolished 14-3-3epsilon-induced in vitro cell proliferation, anchorage-independent growth as well as in vivo tumor growth. Furthermore, AKR1B10 silencing increased retinoic acid (RA) levels in the serum of tumor-bearing mice and RA treatment attenuated 14-3-3epsilon-induced HCC cell proliferation. We further examined 14-3-3epsilon and AKR1B10 expression and clinicopathological characteristics of HCC tumors. Although the expression of AKR1B10 was significantly correlated with 14-3-3epsilon, an increase of AKR1B10 expression in 14-3-3epsilon positive patients paradoxically had better overall survival and disease-free survival rates as well as lower metastatic incidence than those without an AKR1B10 increase. Finally, we found a loss of AKR1B10 expression in cells exhibiting a high capacity of invasiveness. Silencing of AKR1B10 resulted in inducing snail and vimentin expression in HCC cells. These results indicate that AKR1B10 may play a dual role during HCC tumor progression. Our results also indicate that 14-3-3epsilon regulates AKR1B10 expression by activating beta-catenin signaling. A combination of 14-3-3epsilon with AKR1B10 is a potential therapeutic target and novel prognostic biomarker of HCC.
    Date: 2015-11
    Relation: Oncotarget. 2015 Nov;6(36):38967-38982.
    Link to: http://dx.doi.org/10.18632/oncotarget.5734
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000366114000041
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84948808127
    Appears in Collections:[Jun-Yang Liou] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    PUB26516929.pdf6224KbAdobe PDF460View/Open


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

    Related Items in TAIR

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