國家衛生研究院 NHRI:Item 3990099045/10238
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 916376      Online Users : 1422
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
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/10238


    Title: Friend or foe: Role of E-cadherin in prostate cancer metastasis
    Authors: Lin, CY;Chuu, CP
    Contributors: Institute of Cellular and Systems Medicine
    Abstract: Alteration of E-cadherin protein level during epithelial-mesenchymal transition (EMT) or mesenchymal-epithelial transition (MET) plays important role in cancer metastasis (1). In a recent paper “Liver Protects Metastatic Prostate Cancer From Induced Death by Activating E-cadherin Signaling” by Ma et al. (2) reported that the interaction between liver cells and metastatic prostate cancer (PCa) cells provokes re-expression of E-cadherin in PCa cells, which protects PCa cells from cell death induced by chemotherapeutic drugs. E-cadherin fabricates this protection via activation of canonical survival signaling pathways, including the extracellular signal-regulated kinases (ERK), protein kinase B (AKT), and the Janus kinase (JAK) signaling. Ma et al. used DU-145, an androgen-receptor (AR)-negative androgen-independent PCa cell line which expresses very low level of E-cadherin on the cell membrane to determine the role of E-cadherin in PCa chemotherapy resistance. The researchers found that either co-culture with primary hepatocytes to mimic liver cell microenvironment or addition of PD153035 (inhibitor suppressing the kinase activity of epidermal growth factor receptor, EGFR) induced the re-expression of E-cadherin in DU-145. These E-cadherin-high DU-145 cells were much more resistant to chemotherapeutic drugs treatment and TNF-related apoptosis-inducing ligand (TRAIL) both in vitro and in vivo.
    Date: 2016-12
    Relation: Translational Andrology and Urology. 2016 Dec;5(6):961-963.
    Link to: http://dx.doi.org/10.21037/tau.2016.11.08
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2223-4683&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000393291300022
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85006289209
    Appears in Collections:[Chih-Pin Chuu] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    SCP85006289209.pdf195KbAdobe 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