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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31014


    標題: Hinokitiol inhibits vasculogenic mimicry activity of breast cancer stem/progenitor cells through proteasome-mediated degradation of epidermal growth factor receptor
    作者: Tu, Dom-Gene
    Yu, Yun
    Lee, Che-Hsin
    Kuo, Yu-Liang
    Lu, Yin-Che
    Tu, Chi-Wen
    Chang, Wen-Wei
    貢獻者: Chia Yi Christian Hosp, Ditmanson Med Fdn, Dept Nucl Med
    Chia Nan Univ Pharm & Sci, Dept Food Sci & Technol
    Chang Jung Christian Univ, Coll Hlth Sci, Grad Inst Med Sci
    Chung Shan Med Univ, Coll Med Sci & Technol, Sch Biomed Sci
    China Med Univ, Sch Med, Grad Inst Basic Med Sci
    China Med Univ, Sch Med, Dept Microbiol
    Chung Shan Med Univ Hosp, Dept Med Imaging
    Chung Shan Med Univ, Sch Med Imaging & Radiol Sci
    Chia Yi Christian Hosp, Ditmanson Med Fdn, Div Hematol Oncol
    Chia Yi Christian Hosp, Ditmanson Med Fdn, Dept Surg
    Chung Shan Med Univ Hosp, Dept Med Res
    關鍵字: hinokitiol
    vasculogenic mimicry
    breast cancer stem
    progenitor cells
    epidermal growth factor receptor
    differentiation
    日期: 2016-04
    上傳時間: 2018-01-18 11:39:51 (UTC+8)
    出版者: Spandidos Publ Ltd
    摘要: Hinokitiol, alternatively known as -thujaplicin, is a tropolone-associated natural compound with antimicrobial, anti-inflammatory and antitumor activity. Breast cancer stem/progenitor cells (BCSCs) are a subpopulation of breast cancer cells associated with tumor initiation, chemoresistance and metastatic behavior, and may be enriched by mammosphere cultivation. Previous studies have demonstrated that BCSCs exhibit vasculogenic mimicry (VM) activity via the epidermal growth factor receptor (EGFR) signaling pathway. The present study investigated the anti-VM activity of hinokitiol in BCSCs. At a concentration below the half maximal inhibitory concentration, hinokitiol inhibited VM formation of mammosphere cells derived from two human breast cancer cell lines. Hinokitiol was additionally indicated to downregulate EGFR protein expression in mammosphere-forming BCSCs without affecting the expression of messenger RNA. The protein stability of EGFR in BCSCs was also decreased by hinokitiol. The EGFR protein expression and VM formation capability of hinokitiol-treated BCSCs were restored by co-treatment with MG132, a proteasome inhibitor. In conclusion, the present study indicated that hinokitiol may inhibit the VM activity of BCSCs through stimulating proteasome-mediated EGFR degradation. Hinokitiol may act as an anti-VM agent, and may be useful for the development of novel breast cancer therapeutic agents.
    關聯: Oncology Letters, v.11 n.4, pp.2934-2940
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