國家衛生研究院 NHRI:Item 3990099045/12271
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 856895      Online Users : 956
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/3990099045/12271


    Title: Elevated expression of lumican in lung cancer cells promotes bone metastasis through an autocrine regulatory mechanism
    Authors: Liu, KJ;Hsiao, KC;Chu, PY;Chang, GC
    Contributors: National Institute of Cancer Research
    Abstract: Background: The median survival time of lung cancer patients with bone metastasis is less than 6 months. Therefore, reducing the incidence of bone metastasis may provide significant clinical benefits for lung cancer patients. Whole genome expression microarray analysis indicated that the gene encoding for lumican, a protein associated with extracellular matrix interaction, was highly expressed in osteotropic lung cancer cell lines with an enhanced capacity of bone metastasis. Further experiments were conducted to reveal the role of lumican in bone metastasis of lung cancer. Methods: The expression of lumican was suppressed in the osteotropic lung cancer cells and the binding capacity to extracellular matrix components, the in vitro migration and invasion ability, and the in vivo bone metastasis capacity of these cells were examined. Exogenous lumican was provided to investigate the autocrine-regulation mechanism of lumican in the bone metastasis of lung cancer cells. Results: Transfection with lumican specific shRNA in the osteotropic lung cancer cells reduced the establishment of in vivo bone metastasis, but not lung metastasis. Reduction of lumican expression also decreased the attachment of lung osteotropic cancer cells to several extracellular matrix components and suppressed cell migration and invasion in vitro. Exogenous lumican restored these reduced capacities of lumican-knockdown cells and promoted the seeding of lung cancer cells in the bone microenvironment. Conclusion: These results suggest that lumican promotes bone metastasis of lung cancer cells through an autocrine regulatory mechanism and blocking this interaction may provide a new therapeutic approach to reduce bone metastasis in lung cancer.
    Date: 2019-10
    Relation: Annals of Oncology. 2019 Oct;30(Suppl. 6):131.
    Link to: http://dx.doi.org/10.1093/annonc/mdz343.061
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0923-7534&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000491239300282
    Appears in Collections:[Ko-Jiunn Liu] Conference Papers/Meeting Abstract

    Files in This Item:

    File Description SizeFormat
    ISI000491239300282.pdf73KbAdobe PDF246View/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