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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/110720


    Title: EGFR conjunct FSCN1 as a Novel Therapeutic Strategy in Triple-Negative Breast Cancer.
    Authors: Wan, Chao-Qun;Wang, Chao-Qun;Li, Yang;Huang, Bi-Fei;Zh, Yong-Ming;Zhao, Yong-Ming;Yuan, Hui;Guo, Dongfang;Su, Chen-Ming;Hu, Gui-Nv;Wang, Qian;Long, Tengyun;Wang, Yan;湯智昕;Tang, Chih-Hsin;Li, Xiaoni
    Contributors: 生物科技學系
    Date: 2017-11
    Issue Date: 2018-04-03 09:14:11 (UTC+8)
    Abstract: Emerging evidence indicates that Fascin-1 (FSCN1) may possess a causal role in the development
    of several types of cancers and serves as a novel biomarker of aggressiveness in certain carcinomas.
    However, the regulatory mechanism of FSCN1 in triple-negative breast cancer (TNBC) cell invasion
    and migration is still largely unknown. In our study, we observed that the FSCN1 expression rates were
    signifcantly higher in invasive ductal carcinoma, compared with both usual ductal hyperplasia and
    ductal carcinoma in situ. FSCN1 expression was signifcantly higher in cases of TNBC compared with the
    non-TNBC subtype. Overexpression of FSCN1 promoted TNBC cell migration and invasion. Epidermal
    growth factor induced the expression of FSCN1 through activation of MAPK, which subsequently
    promoted cell migration and invasion. A signifcant decrease in FSCN1 expression following the cotreatment
    of FSCN1 siRNA and Geftinib, compared with the separate treatment of FSCN1 siRNA or
    Geftinib. Furthermore, we found that there was a signifcant association between FSCN1 expression
    and poor relapse-free survival and overall survival. Therefore, we suggest that co-targeting epidermal
    growth factor receptor and FSCN1 dual biomarker may be used as a novel therapeutic strategy for
    TNBC.
    Relation: Scientific Reports
    Appears in Collections:[生物科技學系] 期刊論文

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