English  |  正體中文  |  简体中文  |  Items with full text/Total items : 17939/22958 (78%)
Visitors : 7387787      Online Users : 139
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.csmu.edu.tw:8080/ir/handle/310902500/24510


    Title: Soy Isoflavone Genistein Impedes Cancer Stemness and Mesenchymal Transition in Head and Neck Cancer through Activating miR-34a/RTCB Axis
    Authors: Hsieh, PL;Liao, YW;Hsieh, CW;Chen, PN;Yu, CC
    Keywords: cancer stemness;genistein;head and neck cancer;Microrna-34a;RTCB
    Date: 2020
    Issue Date: 2022-08-09T08:03:31Z (UTC)
    Publisher: MDPI
    Abstract: Genistein, a soy-derived phytoestrogen, has been shown to exhibit anti-neoplastic activities in various cancers. Nevertheless, its effects on the elimination of tumor-initiating cells of head and neck cancer (HNC-TICs) remain unclear. Here, we investigated the inhibitory effect of genistein on HNC-TICs and potential mechanisms. Our results demonstrated that genistein lowered the proliferation of HNC-TICs by examining the percentage of ALDH1+ or CD44+ cells. Aside from the downregulation of epithelial-mesenchymal transition (EMT) in HNC-TICs, genistein restricted their tumor propagating capacities in a dose-dependent fashion. Moreover, genistein potentiated cell death caused by three commonly used chemotherapeutic agents (doxorubicin, cisplatin, and 5-FU). Our findings proved that genistein induced ROS production through upregulation of miR-34a, leading to apoptosis in HNC-TICs. The genistein-elicited miR-34a reduced self-renewal, migration, invasion capacities and ALDH1 activity, which may be partly owing to the repression of EMT. Furthermore, we showed that RTCB was a novel target that was negatively regulated by miR-34a and involved in the tumor repressive effect of genistein. Besides, the in vivo study validated that genistein retarded tumor growth through the elevation of miR-34a and suppression of RTCB. These results suggested that genistein-induced miR-34a contributed to the ROS-associated apoptosis and diminished stemness properties via repression of RTCB in HNC-TICs.
    URI: http://dx.doi.org/10.3390/nu12071924
    https://www.webofscience.com/wos/woscc/full-record/WOS:000558015300001
    https://ir.csmu.edu.tw:8080/handle/310902500/24510
    Relation: NUTRIENTS ,2020 ,v12 ,issue 7
    Appears in Collections:[中山醫學大學研究成果] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML204View/Open


    SFX Query

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


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