國家衛生研究院 NHRI:Item 3990099045/7301
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/7301


    Title: Cholestane-3beta, 5alpha, 6beta-triol suppresses proliferation, migration, and invasion of human prostate cancer cells
    Other Titles: Cholestane-3β, 5α, 6β-triol suppresses proliferation, migration, and invasion of human prostate cancer cells
    Authors: Lin, CY;Huo, C;Kuo, LK;Hiipakka, RA;Jones, RB;Lin, HP;Hung, Y;Su, LC;Tseng, JC;Kuo, YY;Wang, YL;Fukui, Y;Kao, YH;Kokontis, JM;Yeh, CC;Chen, LY;Yang, SD;Fu, HH;Chen, YW;Tsai, KKC;Chang, JY;Chuu, CP
    Contributors: Institute of Cellular and Systems Medicine;National Institute of Cancer Research
    Abstract: Oxysterols are oxidation products of cholesterol. 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 ?M caused G1 cell cycle arrest while the TUNEL assay indicated that triol treatment at 20–40 ?M 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 β-actin and α-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.
    Date: 2013-06-13
    Relation: PLoS ONE. 2013 Jun 13;8(6):Article number e65734.
    Link to: http://dx.doi.org/10.1371/journal.pone.0065734
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1932-6203&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000321038800076
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84878980505
    Appears in Collections:[Chih-Pin Chuu] Periodical Articles
    [Yasuhisa Fukui(2010-2016)] Periodical Articles
    [Ya-Wen Chen] Periodical Articles
    [Kelvin Kun-Chih Tsai] Periodical Articles
    [Jang-Yang Chang] Periodical Articles

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