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    ASIA unversity > 管理學院 > 國際企業學系 > 期刊論文 >  Item 310904400/79806


    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/79806


    Title: YC-1 inhibits proliferation of breast cancer cells by downregulating EZH2 expression via activation of c-Cbl and ERK
    Authors: Ling-Chu Chang;Hui-Yi Lin;Meng-Tung Tsai2, Ruey-Hwang Chou;Fang-Yu Lee;Che-Ming Teng;Min-Tsang Hsieh;Hsin-Yi Hung;Li-Jiau Huang;Yung-Luen Yu;Sheng-Chu Kuo
    Contributors: 生物科技學系
    Date: 2014-04
    Issue Date: 2014-06-05 12:11:31 (UTC+8)
    Abstract: Background and Purpose
    YC-1 exhibits potent anticancer activity via numerous actions in many cancer cell lines. Hence, we investigated the in vivo antitumour efficacy of YC-1 in an MDA-MB-468 xenograft model and elucidated the mechanism of down-regulation of enhancer of zeste homology 2 (EZH2) by YC-1 in breast cancer cells.

    Experimental Approach
    In YC–1-treated breast cancer cells and tumour specimens from YC–1-treated MDA-MB-468 xenografts, EZH2 expression was analysed by Western blotting. Pharmacological inhibitors and short hairpin RNA-mediated knockdown were applied to identify possible signalling pathways involved in EZH2 down-regulation by YC-1.

    Key Results
    YC-1 reduced the viability of breast cancer cells and tumour growth in MDA-MB-468 xenografts. In breast cancer cells, YC-1 down-regulated EZH2 expression in a concentration- and time-dependent manner. Depletion of EZH2 reduced the proliferation and susceptibility of breast cancer cells to YC–1-induced apoptosis. EZH2 expression was suppressed in tumour specimens from YC–1-treated MDA-MB-468 xenograft mice. YC-1 enhanced both the degradation rate and ubiquitination of EZH2. The down-regulation of EZH2 by YC-1 was associated with activation of PKA and Src–Raf–ERK-mediated signalling pathways. Furthermore, depletion of Casitas B-lineage lymphoma (c-Cbl), an E3 ubiquitin ligase, abolished YC–1-induced apoptosis and suppression of EZH2. YC-1 rapidly activated c-Cbl to induce signalling associated with ERK and EZH2.

    Conclusion and Implications
    We discovered that YC-1 induces apoptosis and inhibits tumour growth of breast cancer cells via down-regulation of EZH2 by activating c-Cbl and ERK. These data suggest that YC-1 is a potential anticancer drug candidate for triple-negative breast cancer.
    Relation: BRITISH JOURNAL OF PHARMACOLOGY,171(17):4010-4025.
    Appears in Collections:[國際企業學系] 期刊論文

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