Hinokitiol inhibits vasculogenic mimicry activity of breast cancer stem/progenitor cells through proteasome-mediated degradation of epidermal growth factor receptor

doi:10.3892/ol.2016.4300

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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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