National Tsing Hua University Institutional Repository:Cholestane-3β, 5α, 6β-triol Suppresses Proliferation, Migration, and Invasion of Human Prostate Cancer Cells
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    National Tsing Hua University Institutional Repository > 生命科學院  > 生命科學系 > 期刊論文 >  Cholestane-3β, 5α, 6β-triol Suppresses Proliferation, Migration, and Invasion of Human Prostate Cancer Cells


    題名: Cholestane-3β, 5α, 6β-triol Suppresses Proliferation, Migration, and Invasion of Human Prostate Cancer Cells
    作者: Ching-Yu Lin;Chieh Huo;Li-Kuo Kuo;Richard A. Hiipakka;Richard Baker Jones;Hui-Ping Lin;Yuwen Hung;Liang-Cheng Su;Jen-Chih Tseng;Ying-Yu Kuo;Yu-Ling Wang;Yasuhisa Fukui;Yung-Hsi Kao;John M. Kokontis;Chien-Chih Yeh;Linyi Chen;Shiaw-Der Yang;Hsiao-Hui Fu;Ya-Wen Chen;Kelvin K.-C. Tsai;Jang-Yang Chang;Chih-Pin Chuu
    教師: 陳令儀
    日期: 2013
    出版者: Public Library of Science
    關聯: PLoS One, Public Library of Science, Volume 8, Issue 6, JUN 2013, e65734
    關鍵詞: prostate cancer
    EMT markers
    Micro-Western Array
    cell cycle
    摘要: Oxysterols are oxidation products of cholestane-3β, 5α, 6β-triol (abbreviated
    as triol) is one of the most abundant and active oxysterols. Here, we report that triol exhibits
    anti-cancer activity against human prostate cancer cells. Treatment of cells with triol
    dose-dependently suppressed proliferation of LNCaP CDXR-3, DU-145, and PC-3 human
    prostate cancer cells and reduced colony formation in soft agar. Oral administration of triol at 20
    mg/kg daily for three weeks significantly retarded the growth of PC-3 xenografts in nude mice.
    Flow cytometric analysis revealed that triol treatment at 10-40 μM caused G1 cell cycle arrest
    while the TUNEL assay indicated that triol treatment at 20-40 μM induced apoptosis in all three
    cell lines. Micro-Western Arrays and traditional Western blotting methods indicated that triol
    treatment resulted in reduced expression of Akt1, phospho-Akt Ser473, phospho-Akt Thr308,
    PDK1, c-Myc, and Skp2 protein levels as well as accumulation of the cell cycle inhibitor p27Kip.
    Triol treatment also resulted in reduced Akt1 protein expression in PC-3 xenografts.
    Overexpression of Skp2 in PC-3 cells partially rescued the growth inhibition caused by triol.
    Triol treatment suppressed migration and invasion of DU-145, PC-3, and CDXR-3 cells. The
    expression levels of proteins associated with epithelial-mesenchymal transition as well as focal
    adhesion kinase were affected by triol treatment in these cells. Triol treatment caused increased
    expression of E-cadherin protein levels but decreased expression of N-cadherin, vimentin, Slug,
    FAK, phospho-FAK Ser722, and phospho-FAK Tyr861 protein levels. Confocal laser
    microscopy revealed redistribution of beta-actin and alpha-tubulin at the periphery of the CDXR-3 and
    DU-145 cells. Our observations suggest that triol may represent a promising therapeutic agent
    for advanced metastatic prostate cancer.
    顯示於類別:[腦科學研究中心] 期刊論文
    [分子醫學研究所] 期刊論文
    [生命科學系] 期刊論文


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