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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/108423


    Title: CSC-3436 switched tamoxifen-induced autophagy to apoptosis through the inhibition of AMPK/mTOR pathway
    Authors: Way, 魏宗德;Tzong-Der Way;Guang-Huan S;Guang-Huan Sun;Tai-Lung Cha;Tai-Lung Cha;Chien-Chang;Chien-Chang Kao;Sun-Yran Cha;Sun-Yran Chang;Sheng-Chu Ku;Sheng-Chu Kuo;魏宗德;Tzong-Der
    Contributors: 保健營養生技學系
    Date: 2017
    Issue Date: 2017-12-08 14:12:14 (UTC+8)
    Abstract: Background

    Triple-negative breast cancer (TNBC) lacks specific therapeutic target and limits to chemotherapy and is essential to develop novel therapeutic regimens. Increasing studies indicated that tamoxifen, a selective estrogen receptor modulators (SERMs), has anti-tumor therapeutic effect in estrogen receptor α (ERα)-negative tumor. Here, we determined whether autophagy was activated by tamoxifen in TNBC cells. Moreover, CSC-3436 displayed strong and selective growth inhibition on cancer cells. Next, we investigated the anti-proliferation effect of combination of CSC-3436 plus tamoxifen on cell death in TNBC cells.

    Results

    Our study found that tamoxifen induces autophagy in TNBC cells. Endoplasmic reticulum stress and AMPK/mTOR contributed tamoxifen-induced autophagy. Interestingly, in combination treatment with CSC-3436 enhanced the anti-proliferative effect of tamoxifen. We found that CSC-3436 switched tamoxifen-induced autophagy to apoptosis via cleavage of ATG-5. Moreover, AMPK/mTOR pathway may involve in CSC-3436 switched tamoxifen-induced autophagy to apoptosis. The combination of tamoxifen and CSC-3436 produced stronger tumor growth inhibition compared with CSC-3436 or tamoxifen alone treatments in vivo.

    Conclusion

    These data indicated that CSC-3436 combined with tamoxifen may be a potential approach for treatment TNBC.
    Relation: JOURNAL OF BIOMEDICAL SCIENCE
    Appears in Collections:[食品營養與保健生技學系] 期刊論文

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